• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Food For Thought: How Nutrients Affect the Brain
 

Food For Thought: How Nutrients Affect the Brain

on

  • 7,818 views

An overview of nutritional strategies to optimize brain function.

An overview of nutritional strategies to optimize brain function.

Statistics

Views

Total Views
7,818
Views on SlideShare
7,806
Embed Views
12

Actions

Likes
10
Downloads
0
Comments
0

4 Embeds 12

http://www.linkedin.com 8
http://www.pinterest.com 2
http://a0.twimg.com 1
https://www.linkedin.com 1

Accessibility

Upload Details

Uploaded via as Apple Keynote

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment
  • Good Morning! My name is Michael Lara and I’d like to welcome you to day’s seminar, Food For Thought: How Nutrients Affect the Brain. \n\nIn September 1914 Francios was born in San Francisco, the third son of French Immigrants Jean and Jennie. \n\nFrancios was a frail and sickly child growing up in San Francisco, and he was teased mercilessly not only by his two older brothers but also by his classmates. \n\nTo make matters worse, Francios was hopelessly addicted to sugar and junk food. \n\nYoung Francios suffered from headaches, irritability, mood swings and by the time he was 14 he had to drop out of high school. \n\nIt was about that time that he happened to attend a lecture in Oakland on nutrition by Paul Bragg, a self-described health guru and travelling lecturer who advocated better living through nutrition and exercise. \n\nBragg gave a series of talks on the evils of “meat and sugar” in the American diet. \n\nThat lecture had a profound impact on young Francios, and from then on he turned his life around by a religious--some would say even fanatical--attention to diet and exercise. \n\nIn a matter of months Francios transformed himself from a thin, frail adolescent to a strapping young man. He was able to return to High School and join the football team, then went on to earn his Doctor of Chiropractic in San Francisco. \n\nIt was during this time, in the 1930-40’s that Alcatraz Island came to the attention of most Americans, because it was claimed that no one could possibly escape from that fabled penitentary.\n\nBut Francios, invigorated and full of confidence, saw this as a challenge and he vowed to someday make that swim that no other human alive had made--to swim from Alcatraz to San Francisco. \n\nHe began a rigorous program of diet and exercise, and he began doing something that doctors at the time advised patients NOT to do--he began weight training with barbell.\n\nFinally, one cold morning in September around 1950, Francios slipped into the choppy, cold waters just yards away from Alcatraz and began the swim that he had been training for nearly most of his adult life. \n\nHere is Francios making that swim....\n\n\n\n\n\n\n\n\n\n\n
  • So with that introduction, let’s now take a look at what’s in store for us:\n\nIn the first section, nutrition and neurotransmitters, we’ll learn that there’s truth to the old saying, You are what you eat. We ’ll look at how our body use one of the most important macronutrients, protein, and how it transforms it into the the chemical messengers used by our brain. \n\nOn a practical level, we’ll learn how to supplementing with amino acids like tyrosine to improve mood .\n\nIn the second section, Inflammation and Mood, we’ll look at how chronic inflammatory conditions like diabetes are related to cognitive and mood disorders like dementia and depression. Did you know that the next generation of antidepressants are anti-inflammatory drugs? \n\nOn a practical level, we’ll learn about the mood and cognitive enhancing effects of omega-3s, SAMe, and folic acid. \n\nIn the third section, Stress-Related Eating and Appetite, we’ll explore the phenomenon of mindless eating and how it affects the cascade of stress signals originating in the brain. We’ll look at how hormones like cortisol and insulin affect our bodies and our brains, and how they trick us into eating more than we really need. \n\nOn a practical level, we’ll learn how to overcome stress-related eating by using supplements like L-glutamine or diets like the ketogenic diet.\n\nIn the fourth section, Blood Sugar, Brain and Behavior, we’ll take a close look at the how glucose, the brain’s primary fuel source, affects mood and behavior. \n\nOn a practical level, we’ll learn strategies for keeping blood sugar stable. We’ll learn about appetite suppressants like phentermine, and new diet drugs that work by blocking the feel good chemicals associated with eating. We’ll also look at one of the most underutilized weight loss supplements available---psyllium. \n\nIn the fifth and final section, we’ll review strategies on how to optimize attention and sleep. \n\nWe’ll learn about supplements like DMAE that enhance energy and awareness. Finally, I’ll talk about how to combine supplements like melatonin with a light box to optimize sleep and wakefulness. \n\nAt the end of the presentation--if you still haven’t had enough--I’ll give you instructions on how to contact me with any questions you might have about the material I’m going to present today. \n\nSo let’s get started...\n
  • So with that introduction, let’s now take a look at what’s in store for us:\n\nIn the first section, nutrition and neurotransmitters, we’ll learn that there’s truth to the old saying, You are what you eat. We ’ll look at how our body use one of the most important macronutrients, protein, and how it transforms it into the the chemical messengers used by our brain. \n\nOn a practical level, we’ll learn how to supplementing with amino acids like tyrosine to improve mood .\n\nIn the second section, Inflammation and Mood, we’ll look at how chronic inflammatory conditions like diabetes are related to cognitive and mood disorders like dementia and depression. Did you know that the next generation of antidepressants are anti-inflammatory drugs? \n\nOn a practical level, we’ll learn about the mood and cognitive enhancing effects of omega-3s, SAMe, and folic acid. \n\nIn the third section, Stress-Related Eating and Appetite, we’ll explore the phenomenon of mindless eating and how it affects the cascade of stress signals originating in the brain. We’ll look at how hormones like cortisol and insulin affect our bodies and our brains, and how they trick us into eating more than we really need. \n\nOn a practical level, we’ll learn how to overcome stress-related eating by using supplements like L-glutamine or diets like the ketogenic diet.\n\nIn the fourth section, Blood Sugar, Brain and Behavior, we’ll take a close look at the how glucose, the brain’s primary fuel source, affects mood and behavior. \n\nOn a practical level, we’ll learn strategies for keeping blood sugar stable. We’ll learn about appetite suppressants like phentermine, and new diet drugs that work by blocking the feel good chemicals associated with eating. We’ll also look at one of the most underutilized weight loss supplements available---psyllium. \n\nIn the fifth and final section, we’ll review strategies on how to optimize attention and sleep. \n\nWe’ll learn about supplements like DMAE that enhance energy and awareness. Finally, I’ll talk about how to combine supplements like melatonin with a light box to optimize sleep and wakefulness. \n\nAt the end of the presentation--if you still haven’t had enough--I’ll give you instructions on how to contact me with any questions you might have about the material I’m going to present today. \n\nSo let’s get started...\n
  • So with that introduction, let’s now take a look at what’s in store for us:\n\nIn the first section, nutrition and neurotransmitters, we’ll learn that there’s truth to the old saying, You are what you eat. We ’ll look at how our body use one of the most important macronutrients, protein, and how it transforms it into the the chemical messengers used by our brain. \n\nOn a practical level, we’ll learn how to supplementing with amino acids like tyrosine to improve mood .\n\nIn the second section, Inflammation and Mood, we’ll look at how chronic inflammatory conditions like diabetes are related to cognitive and mood disorders like dementia and depression. Did you know that the next generation of antidepressants are anti-inflammatory drugs? \n\nOn a practical level, we’ll learn about the mood and cognitive enhancing effects of omega-3s, SAMe, and folic acid. \n\nIn the third section, Stress-Related Eating and Appetite, we’ll explore the phenomenon of mindless eating and how it affects the cascade of stress signals originating in the brain. We’ll look at how hormones like cortisol and insulin affect our bodies and our brains, and how they trick us into eating more than we really need. \n\nOn a practical level, we’ll learn how to overcome stress-related eating by using supplements like L-glutamine or diets like the ketogenic diet.\n\nIn the fourth section, Blood Sugar, Brain and Behavior, we’ll take a close look at the how glucose, the brain’s primary fuel source, affects mood and behavior. \n\nOn a practical level, we’ll learn strategies for keeping blood sugar stable. We’ll learn about appetite suppressants like phentermine, and new diet drugs that work by blocking the feel good chemicals associated with eating. We’ll also look at one of the most underutilized weight loss supplements available---psyllium. \n\nIn the fifth and final section, we’ll review strategies on how to optimize attention and sleep. \n\nWe’ll learn about supplements like DMAE that enhance energy and awareness. Finally, I’ll talk about how to combine supplements like melatonin with a light box to optimize sleep and wakefulness. \n\nAt the end of the presentation--if you still haven’t had enough--I’ll give you instructions on how to contact me with any questions you might have about the material I’m going to present today. \n\nSo let’s get started...\n
  • So with that introduction, let’s now take a look at what’s in store for us:\n\nIn the first section, nutrition and neurotransmitters, we’ll learn that there’s truth to the old saying, You are what you eat. We ’ll look at how our body use one of the most important macronutrients, protein, and how it transforms it into the the chemical messengers used by our brain. \n\nOn a practical level, we’ll learn how to supplementing with amino acids like tyrosine to improve mood .\n\nIn the second section, Inflammation and Mood, we’ll look at how chronic inflammatory conditions like diabetes are related to cognitive and mood disorders like dementia and depression. Did you know that the next generation of antidepressants are anti-inflammatory drugs? \n\nOn a practical level, we’ll learn about the mood and cognitive enhancing effects of omega-3s, SAMe, and folic acid. \n\nIn the third section, Stress-Related Eating and Appetite, we’ll explore the phenomenon of mindless eating and how it affects the cascade of stress signals originating in the brain. We’ll look at how hormones like cortisol and insulin affect our bodies and our brains, and how they trick us into eating more than we really need. \n\nOn a practical level, we’ll learn how to overcome stress-related eating by using supplements like L-glutamine or diets like the ketogenic diet.\n\nIn the fourth section, Blood Sugar, Brain and Behavior, we’ll take a close look at the how glucose, the brain’s primary fuel source, affects mood and behavior. \n\nOn a practical level, we’ll learn strategies for keeping blood sugar stable. We’ll learn about appetite suppressants like phentermine, and new diet drugs that work by blocking the feel good chemicals associated with eating. We’ll also look at one of the most underutilized weight loss supplements available---psyllium. \n\nIn the fifth and final section, we’ll review strategies on how to optimize attention and sleep. \n\nWe’ll learn about supplements like DMAE that enhance energy and awareness. Finally, I’ll talk about how to combine supplements like melatonin with a light box to optimize sleep and wakefulness. \n\nAt the end of the presentation--if you still haven’t had enough--I’ll give you instructions on how to contact me with any questions you might have about the material I’m going to present today. \n\nSo let’s get started...\n
  • So with that introduction, let’s now take a look at what’s in store for us:\n\nIn the first section, nutrition and neurotransmitters, we’ll learn that there’s truth to the old saying, You are what you eat. We ’ll look at how our body use one of the most important macronutrients, protein, and how it transforms it into the the chemical messengers used by our brain. \n\nOn a practical level, we’ll learn how to supplementing with amino acids like tyrosine to improve mood .\n\nIn the second section, Inflammation and Mood, we’ll look at how chronic inflammatory conditions like diabetes are related to cognitive and mood disorders like dementia and depression. Did you know that the next generation of antidepressants are anti-inflammatory drugs? \n\nOn a practical level, we’ll learn about the mood and cognitive enhancing effects of omega-3s, SAMe, and folic acid. \n\nIn the third section, Stress-Related Eating and Appetite, we’ll explore the phenomenon of mindless eating and how it affects the cascade of stress signals originating in the brain. We’ll look at how hormones like cortisol and insulin affect our bodies and our brains, and how they trick us into eating more than we really need. \n\nOn a practical level, we’ll learn how to overcome stress-related eating by using supplements like L-glutamine or diets like the ketogenic diet.\n\nIn the fourth section, Blood Sugar, Brain and Behavior, we’ll take a close look at the how glucose, the brain’s primary fuel source, affects mood and behavior. \n\nOn a practical level, we’ll learn strategies for keeping blood sugar stable. We’ll learn about appetite suppressants like phentermine, and new diet drugs that work by blocking the feel good chemicals associated with eating. We’ll also look at one of the most underutilized weight loss supplements available---psyllium. \n\nIn the fifth and final section, we’ll review strategies on how to optimize attention and sleep. \n\nWe’ll learn about supplements like DMAE that enhance energy and awareness. Finally, I’ll talk about how to combine supplements like melatonin with a light box to optimize sleep and wakefulness. \n\nAt the end of the presentation--if you still haven’t had enough--I’ll give you instructions on how to contact me with any questions you might have about the material I’m going to present today. \n\nSo let’s get started...\n
  • \nAbout 5 years ago I was asked to see teenage male for attention deficit disorder. His mother had heard of my interest treating psychiatric conditions with supplements, and she called asking if I would see her son, who I’ll call John. \n\nOver the phone, before our first visit, John’s mother described him as a hopeless case of attention deficit, saying that both John and his younger brother were addicted to sugar and bouncing off the walls. \n\nSo you can imagine my surprise when John walks into my office, calmly and serenely, and sits before me...not a sign or symptom of restless or inattention during the hour or so that I interviewed him. \n\nAt the end, I finally had to tell him, “What’s going on, John. Your mother says that you have a severe case of ADD. I don’t see anything like that”\n\nHe said to me, Well did she tell you what she makes us do? \n\nI said that his mother had mentioned amino acid supplements.\n\nHe asked, “Have you ever taken amino Acid supplements” At that point he reaches into his back pack and pulls out a jar of capsule, pours out a fistful and says, “Would you get upset if someone tried to shove this many capsules down your throat first thing in the morning and last thing at night? \n\n\n
  • So let’s begin by considering neurotransmitters, the messenger molecules of the brain that govern almost every function of the body: mood, memory, appetite, sleep...\n\nNeurotransmitters are chemical messengers of the peripheral and central nervous system. \n\nNeurotransmitters function individually and in unison with other neurotransmitters. In fact, they can be likened to the individual instruments of an orchestra. Serotonin, norepinephrine, and dopamine ---much like the brass, woodwinds, and percussion in an orchestra--work in unison: serotonin and dopamine, to enhance mood. Sometimes they complement one another: like NE/5-HT; Sometimes they work in opposition to one another, like the stimulating NT glutamate (turning the volume way up) and the inhibitory NT GABA (turning the volume way down). \n\nSo effective that neurotransmitters are found in some of the most basic forms of life. From an evolutionary perspective, they have been found in the most primitive forms of life--fungus and bacteria; even in organisms without a nervous system. In simple organisms, they work not in communicating from cell to cell, but in communicating with environment. In fact, the first neurotransmitter discovered was acetylcholine at the beginning of the 19th century: it was found in both adrenal glands of animals and in extracts from fungus and bacteria. \n\nSo how do we make neurotransmitters? The answer is simple: we make them from the protein in our diet. \n\nWe recognize 3 classes of macronutrients: fat, protein, and carbohydrates. Of these, protein plays a central role in neurotransmitter synthesis. \n\nProtein is broken down into amino acids: Amino acids are the building blocks of the molecules of life, including neurotransmitters. \n\nPsychopharmacology focuses of altering the effects of neurotransmitters and is very much the cornerstone of contemporary psychiatry. \n\nWe know for example that people with dementia have dysfunction of acetylcholine in frontal cortex. So we use drugs like Aricept to correct this dysfunction.\n\nWe know that people with depression have dysfunction of NE/5-HT in DLPC, and we use drugs like Cymbalta to correct this dysfunction. \n\nBut this idea of targeting drugs to neurotransmitters is a bit simplistic:\n\nMood, memory, appetite and sleep are regulated in a complex interplay of chemical signals: neurotransmitters are not the whole story. \n\nIn our quest for the perfect drug, it’s sometimes easy to overlook the fact that we can immediately alter neurotransmitter function without medication, and we can do that in two ways: \n\nWhat we eat\n\n2) How we move\n
  • So let’s begin by considering neurotransmitters, the messenger molecules of the brain that govern almost every function of the body: mood, memory, appetite, sleep...\n\nNeurotransmitters are chemical messengers of the peripheral and central nervous system. \n\nNeurotransmitters function individually and in unison with other neurotransmitters. In fact, they can be likened to the individual instruments of an orchestra. Serotonin, norepinephrine, and dopamine ---much like the brass, woodwinds, and percussion in an orchestra--work in unison: serotonin and dopamine, to enhance mood. Sometimes they complement one another: like NE/5-HT; Sometimes they work in opposition to one another, like the stimulating NT glutamate (turning the volume way up) and the inhibitory NT GABA (turning the volume way down). \n\nSo effective that neurotransmitters are found in some of the most basic forms of life. From an evolutionary perspective, they have been found in the most primitive forms of life--fungus and bacteria; even in organisms without a nervous system. In simple organisms, they work not in communicating from cell to cell, but in communicating with environment. In fact, the first neurotransmitter discovered was acetylcholine at the beginning of the 19th century: it was found in both adrenal glands of animals and in extracts from fungus and bacteria. \n\nSo how do we make neurotransmitters? The answer is simple: we make them from the protein in our diet. \n\nWe recognize 3 classes of macronutrients: fat, protein, and carbohydrates. Of these, protein plays a central role in neurotransmitter synthesis. \n\nProtein is broken down into amino acids: Amino acids are the building blocks of the molecules of life, including neurotransmitters. \n\nPsychopharmacology focuses of altering the effects of neurotransmitters and is very much the cornerstone of contemporary psychiatry. \n\nWe know for example that people with dementia have dysfunction of acetylcholine in frontal cortex. So we use drugs like Aricept to correct this dysfunction.\n\nWe know that people with depression have dysfunction of NE/5-HT in DLPC, and we use drugs like Cymbalta to correct this dysfunction. \n\nBut this idea of targeting drugs to neurotransmitters is a bit simplistic:\n\nMood, memory, appetite and sleep are regulated in a complex interplay of chemical signals: neurotransmitters are not the whole story. \n\nIn our quest for the perfect drug, it’s sometimes easy to overlook the fact that we can immediately alter neurotransmitter function without medication, and we can do that in two ways: \n\nWhat we eat\n\n2) How we move\n
  • So let’s begin by considering neurotransmitters, the messenger molecules of the brain that govern almost every function of the body: mood, memory, appetite, sleep...\n\nNeurotransmitters are chemical messengers of the peripheral and central nervous system. \n\nNeurotransmitters function individually and in unison with other neurotransmitters. In fact, they can be likened to the individual instruments of an orchestra. Serotonin, norepinephrine, and dopamine ---much like the brass, woodwinds, and percussion in an orchestra--work in unison: serotonin and dopamine, to enhance mood. Sometimes they complement one another: like NE/5-HT; Sometimes they work in opposition to one another, like the stimulating NT glutamate (turning the volume way up) and the inhibitory NT GABA (turning the volume way down). \n\nSo effective that neurotransmitters are found in some of the most basic forms of life. From an evolutionary perspective, they have been found in the most primitive forms of life--fungus and bacteria; even in organisms without a nervous system. In simple organisms, they work not in communicating from cell to cell, but in communicating with environment. In fact, the first neurotransmitter discovered was acetylcholine at the beginning of the 19th century: it was found in both adrenal glands of animals and in extracts from fungus and bacteria. \n\nSo how do we make neurotransmitters? The answer is simple: we make them from the protein in our diet. \n\nWe recognize 3 classes of macronutrients: fat, protein, and carbohydrates. Of these, protein plays a central role in neurotransmitter synthesis. \n\nProtein is broken down into amino acids: Amino acids are the building blocks of the molecules of life, including neurotransmitters. \n\nPsychopharmacology focuses of altering the effects of neurotransmitters and is very much the cornerstone of contemporary psychiatry. \n\nWe know for example that people with dementia have dysfunction of acetylcholine in frontal cortex. So we use drugs like Aricept to correct this dysfunction.\n\nWe know that people with depression have dysfunction of NE/5-HT in DLPC, and we use drugs like Cymbalta to correct this dysfunction. \n\nBut this idea of targeting drugs to neurotransmitters is a bit simplistic:\n\nMood, memory, appetite and sleep are regulated in a complex interplay of chemical signals: neurotransmitters are not the whole story. \n\nIn our quest for the perfect drug, it’s sometimes easy to overlook the fact that we can immediately alter neurotransmitter function without medication, and we can do that in two ways: \n\nWhat we eat\n\n2) How we move\n
  • I mentioned earlier that single neurotransmitters do not control single functions. This diagram helps to explain why. \n\nHere we have three of the most commonly recognized neurotransmitters: Norepinephrine, Serotonin and Dopamine. \n\nNorepinephrine regulates attention, concentration, and energy. \n\nSerotonin regulates obsessions/compulsions and memory. \n\nDopamine regulates pleasure reward and motivation. \n\nBut it’s a little more complicated than that. Neurotransmitters often have functions that overlap. \nIf we consider anxiety, for example, we see that it’s actually regulated by at least two neurotransmitters, Serotonin and Norepinephrine. \n
  • So where do neurotransmitters come from? They originate from the protein in our diet.\n\nProteins, we remember, are made up of amino acids strung together like pearls on a necklace. There are 20 amino acids and they are found in almost every form of life. \n\nAmino acids themselves act as neurotransmitters, or are the direct precursor to neurotransmitters. \n\nAmino acids also make up the membrane receptors on the surface of cell.\n\nThe sequence of amino acids is very important. If just one pearl is out of place, protein necklace does not function.\n\nAn example: An enzyme COMT breaks down NE/DA throughout the brain, especially in prefrontal cortex. We now know that some people who have schizophrenia have a mutation of the enzyme that breaks down catecholamine neurotransmitters. Single substitution of Valine to Methionine. The valine variant breaks down dopamine up to 4 x faster the the methionine variant. \n\nOur bodies can synthesize some of these amino acids acids, but there are others that it can’t; these are called the essential amino acids and our only source for them is the protein in our diet. \n
  • So where do neurotransmitters come from? They originate from the protein in our diet.\n\nProteins, we remember, are made up of amino acids strung together like pearls on a necklace. There are 20 amino acids and they are found in almost every form of life. \n\nAmino acids themselves act as neurotransmitters, or are the direct precursor to neurotransmitters. \n\nAmino acids also make up the membrane receptors on the surface of cell.\n\nThe sequence of amino acids is very important. If just one pearl is out of place, protein necklace does not function.\n\nAn example: An enzyme COMT breaks down NE/DA throughout the brain, especially in prefrontal cortex. We now know that some people who have schizophrenia have a mutation of the enzyme that breaks down catecholamine neurotransmitters. Single substitution of Valine to Methionine. The valine variant breaks down dopamine up to 4 x faster the the methionine variant. \n\nOur bodies can synthesize some of these amino acids acids, but there are others that it can’t; these are called the essential amino acids and our only source for them is the protein in our diet. \n
  • So where do neurotransmitters come from? They originate from the protein in our diet.\n\nProteins, we remember, are made up of amino acids strung together like pearls on a necklace. There are 20 amino acids and they are found in almost every form of life. \n\nAmino acids themselves act as neurotransmitters, or are the direct precursor to neurotransmitters. \n\nAmino acids also make up the membrane receptors on the surface of cell.\n\nThe sequence of amino acids is very important. If just one pearl is out of place, protein necklace does not function.\n\nAn example: An enzyme COMT breaks down NE/DA throughout the brain, especially in prefrontal cortex. We now know that some people who have schizophrenia have a mutation of the enzyme that breaks down catecholamine neurotransmitters. Single substitution of Valine to Methionine. The valine variant breaks down dopamine up to 4 x faster the the methionine variant. \n\nOur bodies can synthesize some of these amino acids acids, but there are others that it can’t; these are called the essential amino acids and our only source for them is the protein in our diet. \n
  • So where do neurotransmitters come from? They originate from the protein in our diet.\n\nProteins, we remember, are made up of amino acids strung together like pearls on a necklace. There are 20 amino acids and they are found in almost every form of life. \n\nAmino acids themselves act as neurotransmitters, or are the direct precursor to neurotransmitters. \n\nAmino acids also make up the membrane receptors on the surface of cell.\n\nThe sequence of amino acids is very important. If just one pearl is out of place, protein necklace does not function.\n\nAn example: An enzyme COMT breaks down NE/DA throughout the brain, especially in prefrontal cortex. We now know that some people who have schizophrenia have a mutation of the enzyme that breaks down catecholamine neurotransmitters. Single substitution of Valine to Methionine. The valine variant breaks down dopamine up to 4 x faster the the methionine variant. \n\nOur bodies can synthesize some of these amino acids acids, but there are others that it can’t; these are called the essential amino acids and our only source for them is the protein in our diet. \n
  • There are 20 amino acids found in nature and we break them down into two types: \n\nEssential and Nonessential. \n\nThe essential amino acids are along the top row of this diagram. These include....\n\nThe non-essential amino acids are listed in gray. These include:....\n\nFrom this diagram we can see some interesting relationships.\n\nThe essential amino acid tryptophan is precursor to serotonin. \n\nThe essential amino acid phenylalanine is precursor to non-essential tyrosine, which in turn makes DA and NE. \n\nWe also see here the branched chain amino acids. \n
  • So let’s step away from building blocks of neurotransmitters and take a look at where the action takes place: in the space between nerve cells, the synaptic cleft. \n\nNerve cell has long tail that connects to an adjacent neuron. The junction where they meet is called a synapse. \n\nChemical message received at cell body is transformed to an electrical impulse that travels down axon. \n
  • Let’s take a closer look at one of the most commonly recognized neurotransmitters, Serotonin. \n\nAssociated with feelings of well-being, but also regulates sleep and appetite. No surprise then that depression is associated with sleep and appetite disturbances. \n\nIt also turns out that 90% of our serotonin is located not in our brain but in our gut, the original nervous system. Most primitive nervous systems found in ...use serotonin as primary chemical messengers. If you think about it we are like those primitive, tubular organisms: basically a tube through which food passes and is absorbed. In one end and out the other. It explains why there is such a high association between digestive disorders like irritable bowel and mood symptoms like depression: the brain and the gut use the same chemical messenger, serotonin. \n\nWe’ve all heard of the tryptophan phenomenon that’s associated with turkey. Tryptophan, we just learned, is the immediate precursor to serotonin. It’s not the absolute amount of tryptophan that matters; its’ the amount of tryptophan relative to other amino acids. Some of the amino acids compete with one another for entry into the brain. Tryptophan competes with phenylalanine and leucine for entry into brain. \n\nFoods with higher ratio (bananas) increase serotonin.\n\nFoods with lower ratio (wheat, rye bread) decrease production of serotonin.\n
  • Let’s take a closer look at one of the most commonly recognized neurotransmitters, Serotonin. \n\nAssociated with feelings of well-being, but also regulates sleep and appetite. No surprise then that depression is associated with sleep and appetite disturbances. \n\nIt also turns out that 90% of our serotonin is located not in our brain but in our gut, the original nervous system. Most primitive nervous systems found in ...use serotonin as primary chemical messengers. If you think about it we are like those primitive, tubular organisms: basically a tube through which food passes and is absorbed. In one end and out the other. It explains why there is such a high association between digestive disorders like irritable bowel and mood symptoms like depression: the brain and the gut use the same chemical messenger, serotonin. \n\nWe’ve all heard of the tryptophan phenomenon that’s associated with turkey. Tryptophan, we just learned, is the immediate precursor to serotonin. It’s not the absolute amount of tryptophan that matters; its’ the amount of tryptophan relative to other amino acids. Some of the amino acids compete with one another for entry into the brain. Tryptophan competes with phenylalanine and leucine for entry into brain. \n\nFoods with higher ratio (bananas) increase serotonin.\n\nFoods with lower ratio (wheat, rye bread) decrease production of serotonin.\n
  • Let’s take a closer look at one of the most commonly recognized neurotransmitters, Serotonin. \n\nAssociated with feelings of well-being, but also regulates sleep and appetite. No surprise then that depression is associated with sleep and appetite disturbances. \n\nIt also turns out that 90% of our serotonin is located not in our brain but in our gut, the original nervous system. Most primitive nervous systems found in ...use serotonin as primary chemical messengers. If you think about it we are like those primitive, tubular organisms: basically a tube through which food passes and is absorbed. In one end and out the other. It explains why there is such a high association between digestive disorders like irritable bowel and mood symptoms like depression: the brain and the gut use the same chemical messenger, serotonin. \n\nWe’ve all heard of the tryptophan phenomenon that’s associated with turkey. Tryptophan, we just learned, is the immediate precursor to serotonin. It’s not the absolute amount of tryptophan that matters; its’ the amount of tryptophan relative to other amino acids. Some of the amino acids compete with one another for entry into the brain. Tryptophan competes with phenylalanine and leucine for entry into brain. \n\nFoods with higher ratio (bananas) increase serotonin.\n\nFoods with lower ratio (wheat, rye bread) decrease production of serotonin.\n
  • Let’s take a closer look at one of the most commonly recognized neurotransmitters, Serotonin. \n\nAssociated with feelings of well-being, but also regulates sleep and appetite. No surprise then that depression is associated with sleep and appetite disturbances. \n\nIt also turns out that 90% of our serotonin is located not in our brain but in our gut, the original nervous system. Most primitive nervous systems found in ...use serotonin as primary chemical messengers. If you think about it we are like those primitive, tubular organisms: basically a tube through which food passes and is absorbed. In one end and out the other. It explains why there is such a high association between digestive disorders like irritable bowel and mood symptoms like depression: the brain and the gut use the same chemical messenger, serotonin. \n\nWe’ve all heard of the tryptophan phenomenon that’s associated with turkey. Tryptophan, we just learned, is the immediate precursor to serotonin. It’s not the absolute amount of tryptophan that matters; its’ the amount of tryptophan relative to other amino acids. Some of the amino acids compete with one another for entry into the brain. Tryptophan competes with phenylalanine and leucine for entry into brain. \n\nFoods with higher ratio (bananas) increase serotonin.\n\nFoods with lower ratio (wheat, rye bread) decrease production of serotonin.\n
  • Let’s take a closer look at one of the most commonly recognized neurotransmitters, Serotonin. \n\nAssociated with feelings of well-being, but also regulates sleep and appetite. No surprise then that depression is associated with sleep and appetite disturbances. \n\nIt also turns out that 90% of our serotonin is located not in our brain but in our gut, the original nervous system. Most primitive nervous systems found in ...use serotonin as primary chemical messengers. If you think about it we are like those primitive, tubular organisms: basically a tube through which food passes and is absorbed. In one end and out the other. It explains why there is such a high association between digestive disorders like irritable bowel and mood symptoms like depression: the brain and the gut use the same chemical messenger, serotonin. \n\nWe’ve all heard of the tryptophan phenomenon that’s associated with turkey. Tryptophan, we just learned, is the immediate precursor to serotonin. It’s not the absolute amount of tryptophan that matters; its’ the amount of tryptophan relative to other amino acids. Some of the amino acids compete with one another for entry into the brain. Tryptophan competes with phenylalanine and leucine for entry into brain. \n\nFoods with higher ratio (bananas) increase serotonin.\n\nFoods with lower ratio (wheat, rye bread) decrease production of serotonin.\n
  • So serotonin is synthesized from the essential amino acid, tryptophan via the enzyme, tryptophan hydroxylase to a compound we have all heard of, and some of us may be already taking as a supplement, 5-HTP. And we can see here that 5-HTP is the immediate precursor to serotonin. \n\nSo you may be asking, if you can take serotonin precursors, why can’t you just take serotonin? The answer has again to do with the blood brain barrier and the stability of serotonin. Serotonin gets broken down by monoamine oxidase. \n\nThat name should ring a bell. Because there is an older class of antidepressants, the monoamine oxidase inhibitors, that inhibit the activity of the enzyme that breaks down serotonin. And if serotonin doesn’t get broken down, then it stays around longer so it can bind to post synaptic receptors and continue to transmit information from cell to cell. \n\nThe problem with inhibiting MAO is that it’s everywhere. \n\nFinally, at the bottom of the slide, we see that breakdown product of serotonin 5-HIAA. \n\nWhat makes this interesting is that at one point scientists were looking for a chemical marker of depression. 5-HIAA was thought to be one marker. It’s found in lower concentrations in the fluid surround the brain (CSF) of suicide victims. First reported 1976 in Archives of General Psychiatry: \n\nThe incidence of suicidal acts was studied in 68 depressed patients and related to the level of 5-hydroxyindoleacetic acid (5HIAA) in the cerebrospinal fluid. The distribution of 5-HIAA levels was bimodal. Patients in the low 5-HIAA mode (below 15 ng/ml) attempted suicide significantly more often than those in the high mode, and they used more violent means. Two of the 20 patients in the low mode, and none of the 48 patients in the high mode died from suicide.\n\n
  • So serotonin is synthesized from the essential amino acid, tryptophan via the enzyme, tryptophan hydroxylase to a compound we have all heard of, and some of us may be already taking as a supplement, 5-HTP. And we can see here that 5-HTP is the immediate precursor to serotonin. \n\nSo you may be asking, if you can take serotonin precursors, why can’t you just take serotonin? The answer has again to do with the blood brain barrier and the stability of serotonin. Serotonin gets broken down by monoamine oxidase. \n\nThat name should ring a bell. Because there is an older class of antidepressants, the monoamine oxidase inhibitors, that inhibit the activity of the enzyme that breaks down serotonin. And if serotonin doesn’t get broken down, then it stays around longer so it can bind to post synaptic receptors and continue to transmit information from cell to cell. \n\nThe problem with inhibiting MAO is that it’s everywhere. \n\nFinally, at the bottom of the slide, we see that breakdown product of serotonin 5-HIAA. \n\nWhat makes this interesting is that at one point scientists were looking for a chemical marker of depression. 5-HIAA was thought to be one marker. It’s found in lower concentrations in the fluid surround the brain (CSF) of suicide victims. First reported 1976 in Archives of General Psychiatry: \n\nThe incidence of suicidal acts was studied in 68 depressed patients and related to the level of 5-hydroxyindoleacetic acid (5HIAA) in the cerebrospinal fluid. The distribution of 5-HIAA levels was bimodal. Patients in the low 5-HIAA mode (below 15 ng/ml) attempted suicide significantly more often than those in the high mode, and they used more violent means. Two of the 20 patients in the low mode, and none of the 48 patients in the high mode died from suicide.\n\n
  • Dopamine is the neurotransmitter most associated with pleasure and reward. The main messengers in the reward pathway of our brain. Whenever we have a pleasurable experience, dopamine circuits (mesolimbic dopamine) light up and dopamine floods the circuitry. \n\nWe just saw that DA is synthesized from essential amino acid phenylalanine, which is converted to tyrosine, which is converted to DA.\n\nIf you inhibit the enzyme tyrosine hyroxylase, tyrosine is not able to convert to dopamine. Drug AMPT does this and is used in experimental models of depression. \n\nLow levels are associated with ADHD, parkinson’s, depression\n\nHigh levels of dopamine are associated with mania, psychosis, and extroversion.\n
  • Dopamine is the neurotransmitter most associated with pleasure and reward. The main messengers in the reward pathway of our brain. Whenever we have a pleasurable experience, dopamine circuits (mesolimbic dopamine) light up and dopamine floods the circuitry. \n\nWe just saw that DA is synthesized from essential amino acid phenylalanine, which is converted to tyrosine, which is converted to DA.\n\nIf you inhibit the enzyme tyrosine hyroxylase, tyrosine is not able to convert to dopamine. Drug AMPT does this and is used in experimental models of depression. \n\nLow levels are associated with ADHD, parkinson’s, depression\n\nHigh levels of dopamine are associated with mania, psychosis, and extroversion.\n
  • Dopamine is the neurotransmitter most associated with pleasure and reward. The main messengers in the reward pathway of our brain. Whenever we have a pleasurable experience, dopamine circuits (mesolimbic dopamine) light up and dopamine floods the circuitry. \n\nWe just saw that DA is synthesized from essential amino acid phenylalanine, which is converted to tyrosine, which is converted to DA.\n\nIf you inhibit the enzyme tyrosine hyroxylase, tyrosine is not able to convert to dopamine. Drug AMPT does this and is used in experimental models of depression. \n\nLow levels are associated with ADHD, parkinson’s, depression\n\nHigh levels of dopamine are associated with mania, psychosis, and extroversion.\n
  • Dopamine is the neurotransmitter most associated with pleasure and reward. The main messengers in the reward pathway of our brain. Whenever we have a pleasurable experience, dopamine circuits (mesolimbic dopamine) light up and dopamine floods the circuitry. \n\nWe just saw that DA is synthesized from essential amino acid phenylalanine, which is converted to tyrosine, which is converted to DA.\n\nIf you inhibit the enzyme tyrosine hyroxylase, tyrosine is not able to convert to dopamine. Drug AMPT does this and is used in experimental models of depression. \n\nLow levels are associated with ADHD, parkinson’s, depression\n\nHigh levels of dopamine are associated with mania, psychosis, and extroversion.\n
  • Dopamine is the neurotransmitter most associated with pleasure and reward. The main messengers in the reward pathway of our brain. Whenever we have a pleasurable experience, dopamine circuits (mesolimbic dopamine) light up and dopamine floods the circuitry. \n\nWe just saw that DA is synthesized from essential amino acid phenylalanine, which is converted to tyrosine, which is converted to DA.\n\nIf you inhibit the enzyme tyrosine hyroxylase, tyrosine is not able to convert to dopamine. Drug AMPT does this and is used in experimental models of depression. \n\nLow levels are associated with ADHD, parkinson’s, depression\n\nHigh levels of dopamine are associated with mania, psychosis, and extroversion.\n
  • When we take a closer look at how dopamine is synthesized, we can see the importance of the essential amino acid Tyrosine. Tyrosine in our diets is converted by the enzyme tyrosine hydroxylase to L-Dopa, which passes the blood brain barrier, and then is converted to Dopamine. If you inhibit the enzyme tyrosine hyroxylase, tyrosine is not able to convert to dopamine. Drug AMPT does this and is used in experimental models of depression.\n\nYou will also notice that Dopamine is the parent to Norepinephrine and Ephinephrine. You can see just how similar they are in chemical structure. \n\nThis is worth keeping in mind because anything that increases dopamine will indirectly affect levels of norepinephrine. It’s also interesting when you consider that that the receptors for norepinephrine have a higher affinity for dopamine than for norepinephrine. \n\nIn the frontal cortex there are no dopamine receptors. When you block norepinephrine, you also get free dopamine. This is one of the ideas behind the drug for ADHD, strattera or atomoxetine. \n\n\nGiven that there’s a lot of interest in figuring out ways to increase dopamine, the topic of supplementing with L-tyrosine comes up. I’ll address that now. \n
  • When we take a closer look at how dopamine is synthesized, we can see the importance of the essential amino acid Tyrosine. Tyrosine in our diets is converted by the enzyme tyrosine hydroxylase to L-Dopa, which passes the blood brain barrier, and then is converted to Dopamine. If you inhibit the enzyme tyrosine hyroxylase, tyrosine is not able to convert to dopamine. Drug AMPT does this and is used in experimental models of depression.\n\nYou will also notice that Dopamine is the parent to Norepinephrine and Ephinephrine. You can see just how similar they are in chemical structure. \n\nThis is worth keeping in mind because anything that increases dopamine will indirectly affect levels of norepinephrine. It’s also interesting when you consider that that the receptors for norepinephrine have a higher affinity for dopamine than for norepinephrine. \n\nIn the frontal cortex there are no dopamine receptors. When you block norepinephrine, you also get free dopamine. This is one of the ideas behind the drug for ADHD, strattera or atomoxetine. \n\n\nGiven that there’s a lot of interest in figuring out ways to increase dopamine, the topic of supplementing with L-tyrosine comes up. I’ll address that now. \n
  • Synthesized from phenylalanine.\n\nDietary sources include chicken, turkey, fish....\n\nWhat makes L-tyrosine interesting is that it’s been studied for its mood and energy enhancing effects. Several studies have found that supplementing with L-tyrosine can help reduce stress, sleep deprivation and can lead to small but significant improvements in cognitive and physical performance. \n\nOf all the amino acids I recommend it seems to be the one that is best tolerated. It doesn’t cause the GI problems that serotonin precursors can cause. \n\nDEMO: Show L-Tyrosine tablets: 2 tablets + Coffee or Green Tea. \n\nI recommend dosing from 1-6 grams per day. Ideal dose is 1-2 grams, three times a day, on an empty stomach, with the last dose being no later than 4:00 pm. \n\n2 grams before a workout to enhance to focus and concentration of aerobic exercise. \n\nSo up to this point we’ve been talking about some of the most commonly recognized neurotransmitters and their precursors. The truth is that S, D, and E are somewhat minor players in the symphony of the brain. Because there is yet another level of control. \n\nThere are two neurotransmitters that act as the central accelerator and brake of the nervous systems: The stimulating, excitatory neurotransmitter Glutamate and the calming, inhibitory neurotrasmitter GABA. \n
  • Synthesized from phenylalanine.\n\nDietary sources include chicken, turkey, fish....\n\nWhat makes L-tyrosine interesting is that it’s been studied for its mood and energy enhancing effects. Several studies have found that supplementing with L-tyrosine can help reduce stress, sleep deprivation and can lead to small but significant improvements in cognitive and physical performance. \n\nOf all the amino acids I recommend it seems to be the one that is best tolerated. It doesn’t cause the GI problems that serotonin precursors can cause. \n\nDEMO: Show L-Tyrosine tablets: 2 tablets + Coffee or Green Tea. \n\nI recommend dosing from 1-6 grams per day. Ideal dose is 1-2 grams, three times a day, on an empty stomach, with the last dose being no later than 4:00 pm. \n\n2 grams before a workout to enhance to focus and concentration of aerobic exercise. \n\nSo up to this point we’ve been talking about some of the most commonly recognized neurotransmitters and their precursors. The truth is that S, D, and E are somewhat minor players in the symphony of the brain. Because there is yet another level of control. \n\nThere are two neurotransmitters that act as the central accelerator and brake of the nervous systems: The stimulating, excitatory neurotransmitter Glutamate and the calming, inhibitory neurotrasmitter GABA. \n
  • Synthesized from phenylalanine.\n\nDietary sources include chicken, turkey, fish....\n\nWhat makes L-tyrosine interesting is that it’s been studied for its mood and energy enhancing effects. Several studies have found that supplementing with L-tyrosine can help reduce stress, sleep deprivation and can lead to small but significant improvements in cognitive and physical performance. \n\nOf all the amino acids I recommend it seems to be the one that is best tolerated. It doesn’t cause the GI problems that serotonin precursors can cause. \n\nDEMO: Show L-Tyrosine tablets: 2 tablets + Coffee or Green Tea. \n\nI recommend dosing from 1-6 grams per day. Ideal dose is 1-2 grams, three times a day, on an empty stomach, with the last dose being no later than 4:00 pm. \n\n2 grams before a workout to enhance to focus and concentration of aerobic exercise. \n\nSo up to this point we’ve been talking about some of the most commonly recognized neurotransmitters and their precursors. The truth is that S, D, and E are somewhat minor players in the symphony of the brain. Because there is yet another level of control. \n\nThere are two neurotransmitters that act as the central accelerator and brake of the nervous systems: The stimulating, excitatory neurotransmitter Glutamate and the calming, inhibitory neurotrasmitter GABA. \n
  • Synthesized from phenylalanine.\n\nDietary sources include chicken, turkey, fish....\n\nWhat makes L-tyrosine interesting is that it’s been studied for its mood and energy enhancing effects. Several studies have found that supplementing with L-tyrosine can help reduce stress, sleep deprivation and can lead to small but significant improvements in cognitive and physical performance. \n\nOf all the amino acids I recommend it seems to be the one that is best tolerated. It doesn’t cause the GI problems that serotonin precursors can cause. \n\nDEMO: Show L-Tyrosine tablets: 2 tablets + Coffee or Green Tea. \n\nI recommend dosing from 1-6 grams per day. Ideal dose is 1-2 grams, three times a day, on an empty stomach, with the last dose being no later than 4:00 pm. \n\n2 grams before a workout to enhance to focus and concentration of aerobic exercise. \n\nSo up to this point we’ve been talking about some of the most commonly recognized neurotransmitters and their precursors. The truth is that S, D, and E are somewhat minor players in the symphony of the brain. Because there is yet another level of control. \n\nThere are two neurotransmitters that act as the central accelerator and brake of the nervous systems: The stimulating, excitatory neurotransmitter Glutamate and the calming, inhibitory neurotrasmitter GABA. \n
  • Gamma amino butryic acid is THE major inhibitory neurotransmitter in the CNS. \n\nIt is the site of action for anti-anxiety medicines like ativan, klonipin, xanax, and valium. We’ll also learn later that supplements like Kava and Valerian interact with GABA receptor. But what is most popular way of affecting GABA? Alcohol. \n\nSynthesized in the brain from glutamate. \n\nGABA taken as a supplement does not enter the brain. \n\nExplain Blood Brain Barrier. \n
  • Gamma amino butryic acid is THE major inhibitory neurotransmitter in the CNS. \n\nIt is the site of action for anti-anxiety medicines like ativan, klonipin, xanax, and valium. We’ll also learn later that supplements like Kava and Valerian interact with GABA receptor. But what is most popular way of affecting GABA? Alcohol. \n\nSynthesized in the brain from glutamate. \n\nGABA taken as a supplement does not enter the brain. \n\nExplain Blood Brain Barrier. \n
  • Gamma amino butryic acid is THE major inhibitory neurotransmitter in the CNS. \n\nIt is the site of action for anti-anxiety medicines like ativan, klonipin, xanax, and valium. We’ll also learn later that supplements like Kava and Valerian interact with GABA receptor. But what is most popular way of affecting GABA? Alcohol. \n\nSynthesized in the brain from glutamate. \n\nGABA taken as a supplement does not enter the brain. \n\nExplain Blood Brain Barrier. \n
  • Gamma amino butryic acid is THE major inhibitory neurotransmitter in the CNS. \n\nIt is the site of action for anti-anxiety medicines like ativan, klonipin, xanax, and valium. We’ll also learn later that supplements like Kava and Valerian interact with GABA receptor. But what is most popular way of affecting GABA? Alcohol. \n\nSynthesized in the brain from glutamate. \n\nGABA taken as a supplement does not enter the brain. \n\nExplain Blood Brain Barrier. \n
  • The major excitatory neurotransmitter.\n\nInvolved in learning and memory. \n\nToo much glutamate can kill cells. Suicide neurotransmitter. \n\nFound in cheese and soy sauce. \n\nThe sensation of taste can be categorized into five basic tastes: sweet, bitter, sour, salty, and umami. “Umami” is originally the Japanese word for “meaty” or “savory”\n\nSodium salt is MSG. \n\nSome anticonvulsant medications are used to stabilize glutamate. Topiramate and Zonisamide thought to moderate glutamate and are actually reduce appetite. \n
  • The major excitatory neurotransmitter.\n\nInvolved in learning and memory. \n\nToo much glutamate can kill cells. Suicide neurotransmitter. \n\nFound in cheese and soy sauce. \n\nThe sensation of taste can be categorized into five basic tastes: sweet, bitter, sour, salty, and umami. “Umami” is originally the Japanese word for “meaty” or “savory”\n\nSodium salt is MSG. \n\nSome anticonvulsant medications are used to stabilize glutamate. Topiramate and Zonisamide thought to moderate glutamate and are actually reduce appetite. \n
  • The major excitatory neurotransmitter.\n\nInvolved in learning and memory. \n\nToo much glutamate can kill cells. Suicide neurotransmitter. \n\nFound in cheese and soy sauce. \n\nThe sensation of taste can be categorized into five basic tastes: sweet, bitter, sour, salty, and umami. “Umami” is originally the Japanese word for “meaty” or “savory”\n\nSodium salt is MSG. \n\nSome anticonvulsant medications are used to stabilize glutamate. Topiramate and Zonisamide thought to moderate glutamate and are actually reduce appetite. \n
  • The major excitatory neurotransmitter.\n\nInvolved in learning and memory. \n\nToo much glutamate can kill cells. Suicide neurotransmitter. \n\nFound in cheese and soy sauce. \n\nThe sensation of taste can be categorized into five basic tastes: sweet, bitter, sour, salty, and umami. “Umami” is originally the Japanese word for “meaty” or “savory”\n\nSodium salt is MSG. \n\nSome anticonvulsant medications are used to stabilize glutamate. Topiramate and Zonisamide thought to moderate glutamate and are actually reduce appetite. \n
  • The major excitatory neurotransmitter.\n\nInvolved in learning and memory. \n\nToo much glutamate can kill cells. Suicide neurotransmitter. \n\nFound in cheese and soy sauce. \n\nThe sensation of taste can be categorized into five basic tastes: sweet, bitter, sour, salty, and umami. “Umami” is originally the Japanese word for “meaty” or “savory”\n\nSodium salt is MSG. \n\nSome anticonvulsant medications are used to stabilize glutamate. Topiramate and Zonisamide thought to moderate glutamate and are actually reduce appetite. \n
  • Within our CNS are scaffolding cells call glia who function is to support and nourish neurons. \n\nThis slide demonstrates how closely the major inhibitory neurotransmitter GABA is related to the major excitatory neurotransmitter Glutamate. \n
  • Within our CNS are scaffolding cells call glia who function is to support and nourish neurons. \n\nThis slide demonstrates how closely the major inhibitory neurotransmitter GABA is related to the major excitatory neurotransmitter Glutamate. \n
  • Within our CNS are scaffolding cells call glia who function is to support and nourish neurons. \n\nThis slide demonstrates how closely the major inhibitory neurotransmitter GABA is related to the major excitatory neurotransmitter Glutamate. \n
  • Within our CNS are scaffolding cells call glia who function is to support and nourish neurons. \n\nThis slide demonstrates how closely the major inhibitory neurotransmitter GABA is related to the major excitatory neurotransmitter Glutamate. \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • So to summarize:\n\nWe’ve learned a little about 5-HT, DA, and NE but we also learned they are not the major players. GABA and Glutamate are major players in CNS. One is synthesized from the other. \n\nThere are now recognized more than 50 compounds that act as neurotransmitters: Nitric Oxide, for example. \n\nI’d like to discuss two more that I will be referring to though out the day: ACh and B-endorphin. \n
  • Ach, like glutamate, involved with learning and short term memory. Neurotransmitter associated and most often targeted in treatment of dementia\n\nSynthesized form B vitamins and choline. \n\nSupplemented with PS and PS. \n\nDementia associated with destruction of cholinergic neurons. \n\nIn my opinion, best way of supplement choline is with DMAE. (100 mg 3x/day)\n\nDEMO DMAE: 100 mgo r 10 drops mixed in caffeine or green tea + 1 gram of L-tyrosine. \n\nTwo other supplements that affect Ach are are Acetyl-L-carnitine (precursor of ACh) and nicotine. \n
  • Ach, like glutamate, involved with learning and short term memory. Neurotransmitter associated and most often targeted in treatment of dementia\n\nSynthesized form B vitamins and choline. \n\nSupplemented with PS and PS. \n\nDementia associated with destruction of cholinergic neurons. \n\nIn my opinion, best way of supplement choline is with DMAE. (100 mg 3x/day)\n\nDEMO DMAE: 100 mgo r 10 drops mixed in caffeine or green tea + 1 gram of L-tyrosine. \n\nTwo other supplements that affect Ach are are Acetyl-L-carnitine (precursor of ACh) and nicotine. \n
  • Ach, like glutamate, involved with learning and short term memory. Neurotransmitter associated and most often targeted in treatment of dementia\n\nSynthesized form B vitamins and choline. \n\nSupplemented with PS and PS. \n\nDementia associated with destruction of cholinergic neurons. \n\nIn my opinion, best way of supplement choline is with DMAE. (100 mg 3x/day)\n\nDEMO DMAE: 100 mgo r 10 drops mixed in caffeine or green tea + 1 gram of L-tyrosine. \n\nTwo other supplements that affect Ach are are Acetyl-L-carnitine (precursor of ACh) and nicotine. \n
  • Ach, like glutamate, involved with learning and short term memory. Neurotransmitter associated and most often targeted in treatment of dementia\n\nSynthesized form B vitamins and choline. \n\nSupplemented with PS and PS. \n\nDementia associated with destruction of cholinergic neurons. \n\nIn my opinion, best way of supplement choline is with DMAE. (100 mg 3x/day)\n\nDEMO DMAE: 100 mgo r 10 drops mixed in caffeine or green tea + 1 gram of L-tyrosine. \n\nTwo other supplements that affect Ach are are Acetyl-L-carnitine (precursor of ACh) and nicotine. \n
  • Ach, like glutamate, involved with learning and short term memory. Neurotransmitter associated and most often targeted in treatment of dementia\n\nSynthesized form B vitamins and choline. \n\nSupplemented with PS and PS. \n\nDementia associated with destruction of cholinergic neurons. \n\nIn my opinion, best way of supplement choline is with DMAE. (100 mg 3x/day)\n\nDEMO DMAE: 100 mgo r 10 drops mixed in caffeine or green tea + 1 gram of L-tyrosine. \n\nTwo other supplements that affect Ach are are Acetyl-L-carnitine (precursor of ACh) and nicotine. \n
  • Ach, like glutamate, involved with learning and short term memory. Neurotransmitter associated and most often targeted in treatment of dementia\n\nSynthesized form B vitamins and choline. \n\nSupplemented with PS and PS. \n\nDementia associated with destruction of cholinergic neurons. \n\nIn my opinion, best way of supplement choline is with DMAE. (100 mg 3x/day)\n\nDEMO DMAE: 100 mgo r 10 drops mixed in caffeine or green tea + 1 gram of L-tyrosine. \n\nTwo other supplements that affect Ach are are Acetyl-L-carnitine (precursor of ACh) and nicotine. \n
  • This slide of a cholinergic neuron illustrates several themes we’ve seen before: \n\nGiven the central role of choline, it’s often suggested as use for enhancing short-term memory. The problem is that it doesn’t get into the brain. \n\nIn my opinion, best way of supplement choline is with DMAE. (100 mg 3x/day) and Acetyl-L-carnitine (500 mg 3x/day).\n\nBruce Ames and Juvenon: $50 for month’s supply. \n\nThe highest doses recommended for acetyl-L-carnitine (no salt specified) and for "-lipoic acid \nare 1,500 and 600 mg/day, respectively\n
  • This slide of a cholinergic neuron illustrates several themes we’ve seen before: \n\nGiven the central role of choline, it’s often suggested as use for enhancing short-term memory. The problem is that it doesn’t get into the brain. \n\nIn my opinion, best way of supplement choline is with DMAE. (100 mg 3x/day) and Acetyl-L-carnitine (500 mg 3x/day).\n\nBruce Ames and Juvenon: $50 for month’s supply. \n\nThe highest doses recommended for acetyl-L-carnitine (no salt specified) and for "-lipoic acid \nare 1,500 and 600 mg/day, respectively\n
  • This slide of a cholinergic neuron illustrates several themes we’ve seen before: \n\nGiven the central role of choline, it’s often suggested as use for enhancing short-term memory. The problem is that it doesn’t get into the brain. \n\nIn my opinion, best way of supplement choline is with DMAE. (100 mg 3x/day) and Acetyl-L-carnitine (500 mg 3x/day).\n\nBruce Ames and Juvenon: $50 for month’s supply. \n\nThe highest doses recommended for acetyl-L-carnitine (no salt specified) and for "-lipoic acid \nare 1,500 and 600 mg/day, respectively\n
  • This slide of a cholinergic neuron illustrates several themes we’ve seen before: \n\nGiven the central role of choline, it’s often suggested as use for enhancing short-term memory. The problem is that it doesn’t get into the brain. \n\nIn my opinion, best way of supplement choline is with DMAE. (100 mg 3x/day) and Acetyl-L-carnitine (500 mg 3x/day).\n\nBruce Ames and Juvenon: $50 for month’s supply. \n\nThe highest doses recommended for acetyl-L-carnitine (no salt specified) and for "-lipoic acid \nare 1,500 and 600 mg/day, respectively\n
  • This slide of a cholinergic neuron illustrates several themes we’ve seen before: \n\nGiven the central role of choline, it’s often suggested as use for enhancing short-term memory. The problem is that it doesn’t get into the brain. \n\nIn my opinion, best way of supplement choline is with DMAE. (100 mg 3x/day) and Acetyl-L-carnitine (500 mg 3x/day).\n\nBruce Ames and Juvenon: $50 for month’s supply. \n\nThe highest doses recommended for acetyl-L-carnitine (no salt specified) and for "-lipoic acid \nare 1,500 and 600 mg/day, respectively\n
  • \n
  • \nThe final neurotransmitter we will consider today are the class known as the endogenous opiates. \n\nBeta endorphin is the main opiate; released during exercise, eating, sex, pain. \n\nProduced in anterior pituitary by cleaving a large peptide 241 amino acid polypeptide into B endorphin and ACTH. \n\nThere is a class of medications that block opiates and they have a number of clinical uses. \n\nBest way to increase endogenous opiates? Aerobic exercise: Sprint training for short periods of time or long distance running for greater than 60 minutes. \n\nNaltrexone blocks the high associated with alcohol abuse. \n\nThey’ve been used for reducing the cutting associated with self-injurious behaviors. \n\nMore recently, class of weight loss drugs that combining drugs that increase NE (wellbutrin) with drugs the block opiates (naltrexone). \n\nSide effects: take away the pleasure associated with other experiences. One study in British Journal of Sports Medicine in 1999 showed that preloading with naltrexone took away subjective high associated with aerobic exercise. \n\n
  • \nThe final neurotransmitter we will consider today are the class known as the endogenous opiates. \n\nBeta endorphin is the main opiate; released during exercise, eating, sex, pain. \n\nProduced in anterior pituitary by cleaving a large peptide 241 amino acid polypeptide into B endorphin and ACTH. \n\nThere is a class of medications that block opiates and they have a number of clinical uses. \n\nBest way to increase endogenous opiates? Aerobic exercise: Sprint training for short periods of time or long distance running for greater than 60 minutes. \n\nNaltrexone blocks the high associated with alcohol abuse. \n\nThey’ve been used for reducing the cutting associated with self-injurious behaviors. \n\nMore recently, class of weight loss drugs that combining drugs that increase NE (wellbutrin) with drugs the block opiates (naltrexone). \n\nSide effects: take away the pleasure associated with other experiences. One study in British Journal of Sports Medicine in 1999 showed that preloading with naltrexone took away subjective high associated with aerobic exercise. \n\n
  • \nThe final neurotransmitter we will consider today are the class known as the endogenous opiates. \n\nBeta endorphin is the main opiate; released during exercise, eating, sex, pain. \n\nProduced in anterior pituitary by cleaving a large peptide 241 amino acid polypeptide into B endorphin and ACTH. \n\nThere is a class of medications that block opiates and they have a number of clinical uses. \n\nBest way to increase endogenous opiates? Aerobic exercise: Sprint training for short periods of time or long distance running for greater than 60 minutes. \n\nNaltrexone blocks the high associated with alcohol abuse. \n\nThey’ve been used for reducing the cutting associated with self-injurious behaviors. \n\nMore recently, class of weight loss drugs that combining drugs that increase NE (wellbutrin) with drugs the block opiates (naltrexone). \n\nSide effects: take away the pleasure associated with other experiences. One study in British Journal of Sports Medicine in 1999 showed that preloading with naltrexone took away subjective high associated with aerobic exercise. \n\n
  • \nThe final neurotransmitter we will consider today are the class known as the endogenous opiates. \n\nBeta endorphin is the main opiate; released during exercise, eating, sex, pain. \n\nProduced in anterior pituitary by cleaving a large peptide 241 amino acid polypeptide into B endorphin and ACTH. \n\nThere is a class of medications that block opiates and they have a number of clinical uses. \n\nBest way to increase endogenous opiates? Aerobic exercise: Sprint training for short periods of time or long distance running for greater than 60 minutes. \n\nNaltrexone blocks the high associated with alcohol abuse. \n\nThey’ve been used for reducing the cutting associated with self-injurious behaviors. \n\nMore recently, class of weight loss drugs that combining drugs that increase NE (wellbutrin) with drugs the block opiates (naltrexone). \n\nSide effects: take away the pleasure associated with other experiences. One study in British Journal of Sports Medicine in 1999 showed that preloading with naltrexone took away subjective high associated with aerobic exercise. \n\n
  • A while back, George, a young silicon valley entrepreneur, came to me seeking help for fatigue and extreme stress.\n\nAt only 35, George was living the fast-paced lifestyle that he thought he needed in order to succeed in his work in Biotech. \n\nWorked 18 hours/day; travelled back and forth to east coast several time a month; constantly fatigued...so much so that he almost boarded a flight to San Fernando instead of San Francisco. \n\nGeorge had been through the usual course of antidepressants and antianxiety medications with his primary care doctor, and he came to me seeking help for his fatigue and stress. He suspected that he might have ADD since his antidepressant and antianxiety medications had not helped. \n\nTo make matters worse, his wife was expecting their first child in a few months. \n\nWhen I asked about physical activity, he said he had no energy. When asked about diet, he said anything and everything. He had gained about 20 lbs in the last several months. \n\nWhat was interesting about his case was that he had access to lab in his company that was investigating cytokines. \n\n I asked if he could get his blood checked for markers of inflammation; he did, and we found that CRP level, marker of inflammation, was high and that he had elevated levels of pro-inflammatory cytokines in his blood; homocysteine levels, a risk factor for heart disease, were off the chart. \n\nInstead of another round of antidepressant medications, I proposed that we start a regimen of omega-3 fatty acids (up to grams/day), that we supplement with high potency prescription B vitamins and a medical food product, a form of Folic Acid called Deplin\n\nAnd just a touch a medication to stabilize his mood and lift his depression, lamotrigine. Lamotrigine works by stabilizing glutamate levels in brain. \n\nWithin months he was sleeping better, less irritabile, and most important: thinking clear that he ever had. better. Still working long hours but more focused. \n\n\n\n
  • TIME magazine cover described inflammation as the silent killer. \n\nNormal response to noxious stimuli. Enabled us to survive. \n\nAcute inflammation v. chronic inflammation. \n\nInflammation is now said to be the cause of not only heart disease but also almost all chronic diseases such as cancer, diabetes, osteoporosis, Alzheimer’s, arthritis, asthma, aging, obesity, etc. The symptoms manifested by inflammation include swelling, tender joints, sore throat, rash, runny nose, blisters, bleeding gums, depression, lethargy, fatigue.\n\nThe inflammatory cascade has its own chemical messengers, including cytokines.\n\nPro-Inflammatory and Anti-inflammatory messengers. Markers and mediators of inflammation: TNF-alpha, IL-6, CRP\n\nCytokines released under various stressful conditions, including sleep deprivation and in response to diet high in refined sugar. \n\nThrough a highly orchestrated and tightly integrated cascade of chemical signaling chronic inflammation can lead to obesity, depression and other chronic diseases. \n\nWhat blood studies can be done to check for Chronic Inflammation? \n\nCRP\n\nFibrinogen: Higher levels are, amongst others, associated with cardiovascular disease (>3.43 g/L). It may be elevated in any form of inflammation, as it is an acute-phase protein; for example, it is especially apparent in human gingival tissue during the initial phase of periodontal disease.[8]\n\nTwo Others: \n\nHemoglobin A1C\n\nHomocysteine: Elevated risk for CAD; Homocysteine is chemically transformed into methionine and cysteine (similar amino acids) with the help of folic acid, vitamin B12, and vitamin B6.\n\n\nLet’s take a closer look at how this process unfold by examining the hypothalamic-pituitary-adrenal axis. \n\n
  • TIME magazine cover described inflammation as the silent killer. \n\nNormal response to noxious stimuli. Enabled us to survive. \n\nAcute inflammation v. chronic inflammation. \n\nInflammation is now said to be the cause of not only heart disease but also almost all chronic diseases such as cancer, diabetes, osteoporosis, Alzheimer’s, arthritis, asthma, aging, obesity, etc. The symptoms manifested by inflammation include swelling, tender joints, sore throat, rash, runny nose, blisters, bleeding gums, depression, lethargy, fatigue.\n\nThe inflammatory cascade has its own chemical messengers, including cytokines.\n\nPro-Inflammatory and Anti-inflammatory messengers. Markers and mediators of inflammation: TNF-alpha, IL-6, CRP\n\nCytokines released under various stressful conditions, including sleep deprivation and in response to diet high in refined sugar. \n\nThrough a highly orchestrated and tightly integrated cascade of chemical signaling chronic inflammation can lead to obesity, depression and other chronic diseases. \n\nWhat blood studies can be done to check for Chronic Inflammation? \n\nCRP\n\nFibrinogen: Higher levels are, amongst others, associated with cardiovascular disease (>3.43 g/L). It may be elevated in any form of inflammation, as it is an acute-phase protein; for example, it is especially apparent in human gingival tissue during the initial phase of periodontal disease.[8]\n\nTwo Others: \n\nHemoglobin A1C\n\nHomocysteine: Elevated risk for CAD; Homocysteine is chemically transformed into methionine and cysteine (similar amino acids) with the help of folic acid, vitamin B12, and vitamin B6.\n\n\nLet’s take a closer look at how this process unfold by examining the hypothalamic-pituitary-adrenal axis. \n\n
  • TIME magazine cover described inflammation as the silent killer. \n\nNormal response to noxious stimuli. Enabled us to survive. \n\nAcute inflammation v. chronic inflammation. \n\nInflammation is now said to be the cause of not only heart disease but also almost all chronic diseases such as cancer, diabetes, osteoporosis, Alzheimer’s, arthritis, asthma, aging, obesity, etc. The symptoms manifested by inflammation include swelling, tender joints, sore throat, rash, runny nose, blisters, bleeding gums, depression, lethargy, fatigue.\n\nThe inflammatory cascade has its own chemical messengers, including cytokines.\n\nPro-Inflammatory and Anti-inflammatory messengers. Markers and mediators of inflammation: TNF-alpha, IL-6, CRP\n\nCytokines released under various stressful conditions, including sleep deprivation and in response to diet high in refined sugar. \n\nThrough a highly orchestrated and tightly integrated cascade of chemical signaling chronic inflammation can lead to obesity, depression and other chronic diseases. \n\nWhat blood studies can be done to check for Chronic Inflammation? \n\nCRP\n\nFibrinogen: Higher levels are, amongst others, associated with cardiovascular disease (>3.43 g/L). It may be elevated in any form of inflammation, as it is an acute-phase protein; for example, it is especially apparent in human gingival tissue during the initial phase of periodontal disease.[8]\n\nTwo Others: \n\nHemoglobin A1C\n\nHomocysteine: Elevated risk for CAD; Homocysteine is chemically transformed into methionine and cysteine (similar amino acids) with the help of folic acid, vitamin B12, and vitamin B6.\n\n\nLet’s take a closer look at how this process unfold by examining the hypothalamic-pituitary-adrenal axis. \n\n
  • TIME magazine cover described inflammation as the silent killer. \n\nNormal response to noxious stimuli. Enabled us to survive. \n\nAcute inflammation v. chronic inflammation. \n\nInflammation is now said to be the cause of not only heart disease but also almost all chronic diseases such as cancer, diabetes, osteoporosis, Alzheimer’s, arthritis, asthma, aging, obesity, etc. The symptoms manifested by inflammation include swelling, tender joints, sore throat, rash, runny nose, blisters, bleeding gums, depression, lethargy, fatigue.\n\nThe inflammatory cascade has its own chemical messengers, including cytokines.\n\nPro-Inflammatory and Anti-inflammatory messengers. Markers and mediators of inflammation: TNF-alpha, IL-6, CRP\n\nCytokines released under various stressful conditions, including sleep deprivation and in response to diet high in refined sugar. \n\nThrough a highly orchestrated and tightly integrated cascade of chemical signaling chronic inflammation can lead to obesity, depression and other chronic diseases. \n\nWhat blood studies can be done to check for Chronic Inflammation? \n\nCRP\n\nFibrinogen: Higher levels are, amongst others, associated with cardiovascular disease (>3.43 g/L). It may be elevated in any form of inflammation, as it is an acute-phase protein; for example, it is especially apparent in human gingival tissue during the initial phase of periodontal disease.[8]\n\nTwo Others: \n\nHemoglobin A1C\n\nHomocysteine: Elevated risk for CAD; Homocysteine is chemically transformed into methionine and cysteine (similar amino acids) with the help of folic acid, vitamin B12, and vitamin B6.\n\n\nLet’s take a closer look at how this process unfold by examining the hypothalamic-pituitary-adrenal axis. \n\n
  • TIME magazine cover described inflammation as the silent killer. \n\nNormal response to noxious stimuli. Enabled us to survive. \n\nAcute inflammation v. chronic inflammation. \n\nInflammation is now said to be the cause of not only heart disease but also almost all chronic diseases such as cancer, diabetes, osteoporosis, Alzheimer’s, arthritis, asthma, aging, obesity, etc. The symptoms manifested by inflammation include swelling, tender joints, sore throat, rash, runny nose, blisters, bleeding gums, depression, lethargy, fatigue.\n\nThe inflammatory cascade has its own chemical messengers, including cytokines.\n\nPro-Inflammatory and Anti-inflammatory messengers. Markers and mediators of inflammation: TNF-alpha, IL-6, CRP\n\nCytokines released under various stressful conditions, including sleep deprivation and in response to diet high in refined sugar. \n\nThrough a highly orchestrated and tightly integrated cascade of chemical signaling chronic inflammation can lead to obesity, depression and other chronic diseases. \n\nWhat blood studies can be done to check for Chronic Inflammation? \n\nCRP\n\nFibrinogen: Higher levels are, amongst others, associated with cardiovascular disease (>3.43 g/L). It may be elevated in any form of inflammation, as it is an acute-phase protein; for example, it is especially apparent in human gingival tissue during the initial phase of periodontal disease.[8]\n\nTwo Others: \n\nHemoglobin A1C\n\nHomocysteine: Elevated risk for CAD; Homocysteine is chemically transformed into methionine and cysteine (similar amino acids) with the help of folic acid, vitamin B12, and vitamin B6.\n\n\nLet’s take a closer look at how this process unfold by examining the hypothalamic-pituitary-adrenal axis. \n\n
  • Normally in response to stress, the hypothalamus release CRH, the pituitary releases ACTH, which then leaves the brain and travels to target organs like the adrenal glands, which release epinephrine. In prep for the flight-or-fight response. \n\n\nThe Trier Social Stress Test (TSST) is a standardized laboratory psychosocial stress test that reliably activates the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system.. More recently, the TSST has also been shown to activate inflammatory signaling pathways and to stimulate pro inflammatory cytokine production in healthy adults \n\n\n\n\n
  • \nSo we just saw how HPA modulates reactions to stress...\n\nCortisol is a key player in this cascade. Produced by adrenal gland, cortisol regulates blood sugar and suppresses acute inflammation. \n\nAddison’s disease=adrenal insufficiency=low cortisol; Symptoms include fatigue, muscle weakness. Body is unable to mount a reaction to stress. John Kennedy suffered from Addison’s. \n\nAltered cortisol secretion is seen in MDD and PTSD. Overactivity of this system thought to be a marker for depression. \n\nSalivary Cortisol Levels: Levels check 4x/day. \n\nDexamethasone suppression test: 1 mg dexamethasone at 11:00 pm-midnight; take serum cortisol level between 7-9 the next morning. Values of greater than 2 picograms/dl suggest endogenous depression.\n\nSo let’s take a look at an example of how this works....\n
  • \nSo we just saw how HPA modulates reactions to stress...\n\nCortisol is a key player in this cascade. Produced by adrenal gland, cortisol regulates blood sugar and suppresses acute inflammation. \n\nAddison’s disease=adrenal insufficiency=low cortisol; Symptoms include fatigue, muscle weakness. Body is unable to mount a reaction to stress. John Kennedy suffered from Addison’s. \n\nAltered cortisol secretion is seen in MDD and PTSD. Overactivity of this system thought to be a marker for depression. \n\nSalivary Cortisol Levels: Levels check 4x/day. \n\nDexamethasone suppression test: 1 mg dexamethasone at 11:00 pm-midnight; take serum cortisol level between 7-9 the next morning. Values of greater than 2 picograms/dl suggest endogenous depression.\n\nSo let’s take a look at an example of how this works....\n
  • \nSo we just saw how HPA modulates reactions to stress...\n\nCortisol is a key player in this cascade. Produced by adrenal gland, cortisol regulates blood sugar and suppresses acute inflammation. \n\nAddison’s disease=adrenal insufficiency=low cortisol; Symptoms include fatigue, muscle weakness. Body is unable to mount a reaction to stress. John Kennedy suffered from Addison’s. \n\nAltered cortisol secretion is seen in MDD and PTSD. Overactivity of this system thought to be a marker for depression. \n\nSalivary Cortisol Levels: Levels check 4x/day. \n\nDexamethasone suppression test: 1 mg dexamethasone at 11:00 pm-midnight; take serum cortisol level between 7-9 the next morning. Values of greater than 2 picograms/dl suggest endogenous depression.\n\nSo let’s take a look at an example of how this works....\n
  • \nSo we just saw how HPA modulates reactions to stress...\n\nCortisol is a key player in this cascade. Produced by adrenal gland, cortisol regulates blood sugar and suppresses acute inflammation. \n\nAddison’s disease=adrenal insufficiency=low cortisol; Symptoms include fatigue, muscle weakness. Body is unable to mount a reaction to stress. John Kennedy suffered from Addison’s. \n\nAltered cortisol secretion is seen in MDD and PTSD. Overactivity of this system thought to be a marker for depression. \n\nSalivary Cortisol Levels: Levels check 4x/day. \n\nDexamethasone suppression test: 1 mg dexamethasone at 11:00 pm-midnight; take serum cortisol level between 7-9 the next morning. Values of greater than 2 picograms/dl suggest endogenous depression.\n\nSo let’s take a look at an example of how this works....\n
  • Stress could come from any number of sources:\n\nHypothalamus sends CRH to Pituitary, which is located outside BB barrier.\n\nAdrenal gland releases cortisol, which has a negative feedback on hypothalamus and pituitary. \n
  • The link between depression and inflammation is seen in phenomenon of “sickness behavior” in which mammals, when given inflammatory cytokines, adopt behavior consistent with depression: fatigue, social withdrawal. In humans, we see this happen with patients who are being treated with interferon alpha for hepatitis. \n\nPatients who are depressed also show an increased in inflammatory cytokines IL-6, TNF alpha, and C-reactive protein. \n\nAll these cytokines upregulate the HPA axis, increasing cortisol in brain. \n\n\n
  • The link between depression and inflammation is seen in phenomenon of “sickness behavior” in which mammals, when given inflammatory cytokines, adopt behavior consistent with depression: fatigue, social withdrawal. In humans, we see this happen with patients who are being treated with interferon alpha for hepatitis. \n\nPatients who are depressed also show an increased in inflammatory cytokines IL-6, TNF alpha, and C-reactive protein. \n\nAll these cytokines upregulate the HPA axis, increasing cortisol in brain. \n\n\n
  • The link between depression and inflammation is seen in phenomenon of “sickness behavior” in which mammals, when given inflammatory cytokines, adopt behavior consistent with depression: fatigue, social withdrawal. In humans, we see this happen with patients who are being treated with interferon alpha for hepatitis. \n\nPatients who are depressed also show an increased in inflammatory cytokines IL-6, TNF alpha, and C-reactive protein. \n\nAll these cytokines upregulate the HPA axis, increasing cortisol in brain. \n\n\n
  • The link between depression and inflammation is seen in phenomenon of “sickness behavior” in which mammals, when given inflammatory cytokines, adopt behavior consistent with depression: fatigue, social withdrawal. In humans, we see this happen with patients who are being treated with interferon alpha for hepatitis. \n\nPatients who are depressed also show an increased in inflammatory cytokines IL-6, TNF alpha, and C-reactive protein. \n\nAll these cytokines upregulate the HPA axis, increasing cortisol in brain. \n\n\n
  • The link between depression and inflammation is seen in phenomenon of “sickness behavior” in which mammals, when given inflammatory cytokines, adopt behavior consistent with depression: fatigue, social withdrawal. In humans, we see this happen with patients who are being treated with interferon alpha for hepatitis. \n\nPatients who are depressed also show an increased in inflammatory cytokines IL-6, TNF alpha, and C-reactive protein. \n\nAll these cytokines upregulate the HPA axis, increasing cortisol in brain. \n\n\n
  • This slide shows the effects of chronically elevated cortisol on one area of the brain responsible for short term memory, the hippocampus. Normal sized hippocampus v. hippocampus in depressed patient. \n\n\n
  • This slide shows the effects of chronically elevated cortisol on one area of the brain responsible for short term memory, the hippocampus. Normal sized hippocampus v. hippocampus in depressed patient. \n\n\n
  • This slide shows the effects of chronically elevated cortisol on one area of the brain responsible for short term memory, the hippocampus. Normal sized hippocampus v. hippocampus in depressed patient. \n\n\n
  • This slide shows the effects of chronically elevated cortisol on one area of the brain responsible for short term memory, the hippocampus. Normal sized hippocampus v. hippocampus in depressed patient. \n\n\n
  • DEMO: Telomeres Shortening and Mood Disorders \n\nBackground: The hypothalamic-pituitary-adrenal(HPA)axisplays a central role in stress regulation,and leukocyte telomere length(TL)has been suggested to represent a cumulative measure of stress. Depression is intimately related with stress and frequently exhibits a dysregulated HPA axis. We aimed to study the relationships between TL and biological and psychological facets of stress in recurrent major depressive disorder and controls.\n\nMethods: Leukocyte TL was measured in 91subjects with recurrent major depressive disorder and 451control subjects.Stress was assessed from both a biological perspective, by assessing HPA axis function with a weight-adjusted very-low-dose dexamethasone suppression test (DST), and a psychological perspective, with self-report questionnaires.\n\nResults: TL was shorter among patients compared with control subjects (277 base pairs, p .001). Overall, short TL was associated with a hypocortisolemic state (low post-DST cortisol and high percentage of cortisol reduction after the DST) among both patients and control subjects but more pronounced among patients. This state, which was overrepresented among patients, was characterized by high familial loading of affective disorders among patients ( p .001) and high C-reactive protein levels among control subjects ( p .040). TL was also inversely associated with stress measured with the Perceived Stress Questionnaire ( rs .258, p .003\n
  • Telomere Shortening and Mood Disorders:\nPreliminary Support for a Chronic Stress Model of Accelerated Aging\n\nNaomi M. Simon, Jordan W. Smoller \n\nBackground: Little is known about the biological mechanisms underlying the excess medical morbidity and mortality associated with mood disorders. Substantial evidence supports abnormalities in stress-related biological systems in depression. Accelerated telomere shortening may reflect stress-related oxidative damage to cells and accelerated aging, and severe psychosocial stress has been linked to telomere shortening. We propose that chronic stress associated with mood disorders may contribute to excess vulnerability for diseases of aging such as cardiovascular disease and possibly some cancers through accelerated organismal aging.\n\nMethods: Telomere length was measured by Southern Analysis in 44 individuals with chronic mood disorders and 44 nonpsychiatrically ill age-matched control subjects.\nResults: Telomere length was significantly shorter in those with mood disorders, representing as much as 10 years of accelerated aging.\nConclusions: These results provide preliminary evidence that mood disorders are associated with accelerated aging and may suggest a novel mechanism for mood disorder-associated morbidity and mortality.\n1. Simon N, Smoller J, McNamara K, al E. Telomere shortening and mood disorders: preliminary support for a chronic stress model of accelerated aging. … psychiatry. 2006.\n
  • The link between depression and inflammation is strengthened when we see that drugs that block or cytokines can reverse depression. AD in particular have been shown to decrease the production of inflammatory cytokines (interferon gamma) and increase the production of ant-inflammatory cytokines (IL-10). \n\nRecent studies: Anti-inflammatories reduce the risk of antidepressants. \n
  • Some evidence that suggests depression linked to inflammation; even more compelling that Alzheimer’s is caused by chronic inflammation. \n\nAlzheimer’s is most common form of dementia. \n\nBelieved to be caused by accumulation of beta amyloid plaques and tau proteins. \n\nOne other consistent finding in patients with Alzheimer’s is overproduction of inflammatory cytokines. \n\nSome studies have suggested that NSAIDs may protect against AD.\n\n\n
  • Some evidence that suggests depression linked to inflammation; even more compelling that Alzheimer’s is caused by chronic inflammation. \n\nAlzheimer’s is most common form of dementia. \n\nBelieved to be caused by accumulation of beta amyloid plaques and tau proteins. \n\nOne other consistent finding in patients with Alzheimer’s is overproduction of inflammatory cytokines. \n\nSome studies have suggested that NSAIDs may protect against AD.\n\n\n
  • Some evidence that suggests depression linked to inflammation; even more compelling that Alzheimer’s is caused by chronic inflammation. \n\nAlzheimer’s is most common form of dementia. \n\nBelieved to be caused by accumulation of beta amyloid plaques and tau proteins. \n\nOne other consistent finding in patients with Alzheimer’s is overproduction of inflammatory cytokines. \n\nSome studies have suggested that NSAIDs may protect against AD.\n\n\n
  • Some evidence that suggests depression linked to inflammation; even more compelling that Alzheimer’s is caused by chronic inflammation. \n\nAlzheimer’s is most common form of dementia. \n\nBelieved to be caused by accumulation of beta amyloid plaques and tau proteins. \n\nOne other consistent finding in patients with Alzheimer’s is overproduction of inflammatory cytokines. \n\nSome studies have suggested that NSAIDs may protect against AD.\n\n\n
  • \n
  • \n
  • Evidence that AD spreads from cells of entorhinal cortex to other cells, like an an infection. \n
  • \n
  • So if chronic system inflammation is the common denominator of chronic diseases like depression and dementia, what can we do to prevent it? \n\nAnswer is to avoid food that cause it, and consume more anti-inflammatory nutrients. \n\nMediterranean Diet: In fact, a recent analysis of more than 1.5 million healthy adults demonstrated that following a Mediterranean diet was associated with a reduced risk of overall and cardiovascular mortality, a reduced incidence of cancer and cancer mortality, and a reduced incidence of Parkinson's and Alzheimer's diseases.\n\nThe principal aspects of this diet include high olive oil consumption, high consumption of legumes, high consumption of unrefined cereals, high consumption of fruits, high consumption of vegetables, moderate consumption of dairy products (mostly as cheese and yogurt), moderate to high consumption of fish, low consumption of meat and meat products, and moderate wine consumption.\n
  • So if chronic system inflammation is the common denominator of chronic diseases like depression and dementia, what can we do to prevent it? \n\nAnswer is to avoid food that cause it, and consume more anti-inflammatory nutrients. \n\nMediterranean Diet: In fact, a recent analysis of more than 1.5 million healthy adults demonstrated that following a Mediterranean diet was associated with a reduced risk of overall and cardiovascular mortality, a reduced incidence of cancer and cancer mortality, and a reduced incidence of Parkinson's and Alzheimer's diseases.\n\nThe principal aspects of this diet include high olive oil consumption, high consumption of legumes, high consumption of unrefined cereals, high consumption of fruits, high consumption of vegetables, moderate consumption of dairy products (mostly as cheese and yogurt), moderate to high consumption of fish, low consumption of meat and meat products, and moderate wine consumption.\n
  • So if chronic system inflammation is the common denominator of chronic diseases like depression and dementia, what can we do to prevent it? \n\nAnswer is to avoid food that cause it, and consume more anti-inflammatory nutrients. \n\nMediterranean Diet: In fact, a recent analysis of more than 1.5 million healthy adults demonstrated that following a Mediterranean diet was associated with a reduced risk of overall and cardiovascular mortality, a reduced incidence of cancer and cancer mortality, and a reduced incidence of Parkinson's and Alzheimer's diseases.\n\nThe principal aspects of this diet include high olive oil consumption, high consumption of legumes, high consumption of unrefined cereals, high consumption of fruits, high consumption of vegetables, moderate consumption of dairy products (mostly as cheese and yogurt), moderate to high consumption of fish, low consumption of meat and meat products, and moderate wine consumption.\n
  • So if chronic system inflammation is the common denominator of chronic diseases like depression and dementia, what can we do to prevent it? \n\nAnswer is to avoid food that cause it, and consume more anti-inflammatory nutrients. \n\nMediterranean Diet: In fact, a recent analysis of more than 1.5 million healthy adults demonstrated that following a Mediterranean diet was associated with a reduced risk of overall and cardiovascular mortality, a reduced incidence of cancer and cancer mortality, and a reduced incidence of Parkinson's and Alzheimer's diseases.\n\nThe principal aspects of this diet include high olive oil consumption, high consumption of legumes, high consumption of unrefined cereals, high consumption of fruits, high consumption of vegetables, moderate consumption of dairy products (mostly as cheese and yogurt), moderate to high consumption of fish, low consumption of meat and meat products, and moderate wine consumption.\n
  • So if chronic system inflammation is the common denominator of chronic diseases like depression and dementia, what can we do to prevent it? \n\nAnswer is to avoid food that cause it, and consume more anti-inflammatory nutrients. \n\nMediterranean Diet: In fact, a recent analysis of more than 1.5 million healthy adults demonstrated that following a Mediterranean diet was associated with a reduced risk of overall and cardiovascular mortality, a reduced incidence of cancer and cancer mortality, and a reduced incidence of Parkinson's and Alzheimer's diseases.\n\nThe principal aspects of this diet include high olive oil consumption, high consumption of legumes, high consumption of unrefined cereals, high consumption of fruits, high consumption of vegetables, moderate consumption of dairy products (mostly as cheese and yogurt), moderate to high consumption of fish, low consumption of meat and meat products, and moderate wine consumption.\n
  • So if chronic system inflammation is the common denominator of chronic diseases like depression and dementia, what can we do to prevent it? \n\nAnswer is to avoid food that cause it, and consume more anti-inflammatory nutrients. \n\nMediterranean Diet: In fact, a recent analysis of more than 1.5 million healthy adults demonstrated that following a Mediterranean diet was associated with a reduced risk of overall and cardiovascular mortality, a reduced incidence of cancer and cancer mortality, and a reduced incidence of Parkinson's and Alzheimer's diseases.\n\nThe principal aspects of this diet include high olive oil consumption, high consumption of legumes, high consumption of unrefined cereals, high consumption of fruits, high consumption of vegetables, moderate consumption of dairy products (mostly as cheese and yogurt), moderate to high consumption of fish, low consumption of meat and meat products, and moderate wine consumption.\n
  • \n\nA study published in the Archives of General Psychiatry shows that people who followed the Mediterranean diet were less likely to develop depression.\n\nA 2008 study published in The New England Journal of Medicine examined the effects of three diets: low-carb, low-fat, and Mediterranean. The study involved 322 participants and lasted for two years. The low-carb and Mediterranean diet resulted in the greatest weight loss, 12 lbs and 10 lbs, respectively. The low-fat diet resulted in a loss of 7 lbs. One caveat of the study is that 86% of the study participants were men. The low-carb and Mediterranean diets produced similar amounts of weight loss in the overall study results and in the men. In the remaining participants who were women, the Mediterranean diet produced 3.8 kg (8.4 lbs) more weight loss on average than the low-carb diet\n
  • \nA total of 2,258 community-based nondemented individuals in New York were prospectively evaluated every 1.5 years. Adherence to the MeDi (zero- to nine-point scale with higher scores indicating higher adherence) was the main predictor in models that were adjusted for cohort, age, sex, ethnicity, education, apolipoprotein E genotype, caloric intake, smoking, medical comorbidity index, and body mass index.\n\nSurvival curves based on Cox analysis comparing cumulative Alzheimer’s disease (AD)incidence in subjects belonging to each Mediterranean diet (MeDi) tertile (p for trend =0.007). Low tertile (score 0–3; light gray lines) corresponds to lower adherence to MeDi,middle tertile (score 4–5; dark gray lines) to middle adherence, and high tertile (score 6–9;black lines) to higher adherence. Figure is derived from a model that uses all subjects and is adjusted for cohort, age, sex, ethnicity, education, apolipoprotein E genotype, caloric intake,smoking, comorbidity index, and body mass index. Duration of follow-up is truncated at 10 years\n
  • About 80 years ago the ratio of omega 6 to omega 3 in our diets was about 1:1, and now it is about 20:1. Omega 6s: corn, soy, safflower. \n\nIt has been suggested that n 2 3 fatty acids [ a -linolenic acid (ALA), eicosapentaenoic acid (EP A), docosa- pentaenoic acid (DP A n 2 3), and docosahexaenoic acid (DHA)] have become less abundant in American diets, and the average ratio of n 2 6t on 2 3 fatty acids has increased from as little as 1:1 to as much as 30:1 \n\nPer capita consumption of soybean oil, for example, increased by more than a 1,000 fold from 1909-1999.\n\nEPA, DHA, ALA\n\nCommon sources: breast milk...\n\nMaintain fluidity of cell membrane and stabilize blood glucose. Also play key role in making anti-inflammatory signals. \n
  • About 80 years ago the ratio of omega 6 to omega 3 in our diets was about 1:1, and now it is about 20:1. Omega 6s: corn, soy, safflower. \n\nIt has been suggested that n 2 3 fatty acids [ a -linolenic acid (ALA), eicosapentaenoic acid (EP A), docosa- pentaenoic acid (DP A n 2 3), and docosahexaenoic acid (DHA)] have become less abundant in American diets, and the average ratio of n 2 6t on 2 3 fatty acids has increased from as little as 1:1 to as much as 30:1 \n\nPer capita consumption of soybean oil, for example, increased by more than a 1,000 fold from 1909-1999.\n\nEPA, DHA, ALA\n\nCommon sources: breast milk...\n\nMaintain fluidity of cell membrane and stabilize blood glucose. Also play key role in making anti-inflammatory signals. \n
  • About 80 years ago the ratio of omega 6 to omega 3 in our diets was about 1:1, and now it is about 20:1. Omega 6s: corn, soy, safflower. \n\nIt has been suggested that n 2 3 fatty acids [ a -linolenic acid (ALA), eicosapentaenoic acid (EP A), docosa- pentaenoic acid (DP A n 2 3), and docosahexaenoic acid (DHA)] have become less abundant in American diets, and the average ratio of n 2 6t on 2 3 fatty acids has increased from as little as 1:1 to as much as 30:1 \n\nPer capita consumption of soybean oil, for example, increased by more than a 1,000 fold from 1909-1999.\n\nEPA, DHA, ALA\n\nCommon sources: breast milk...\n\nMaintain fluidity of cell membrane and stabilize blood glucose. Also play key role in making anti-inflammatory signals. \n
  • About 80 years ago the ratio of omega 6 to omega 3 in our diets was about 1:1, and now it is about 20:1. Omega 6s: corn, soy, safflower. \n\nIt has been suggested that n 2 3 fatty acids [ a -linolenic acid (ALA), eicosapentaenoic acid (EP A), docosa- pentaenoic acid (DP A n 2 3), and docosahexaenoic acid (DHA)] have become less abundant in American diets, and the average ratio of n 2 6t on 2 3 fatty acids has increased from as little as 1:1 to as much as 30:1 \n\nPer capita consumption of soybean oil, for example, increased by more than a 1,000 fold from 1909-1999.\n\nEPA, DHA, ALA\n\nCommon sources: breast milk...\n\nMaintain fluidity of cell membrane and stabilize blood glucose. Also play key role in making anti-inflammatory signals. \n
  • About 80 years ago the ratio of omega 6 to omega 3 in our diets was about 1:1, and now it is about 20:1. Omega 6s: corn, soy, safflower. \n\nIt has been suggested that n 2 3 fatty acids [ a -linolenic acid (ALA), eicosapentaenoic acid (EP A), docosa- pentaenoic acid (DP A n 2 3), and docosahexaenoic acid (DHA)] have become less abundant in American diets, and the average ratio of n 2 6t on 2 3 fatty acids has increased from as little as 1:1 to as much as 30:1 \n\nPer capita consumption of soybean oil, for example, increased by more than a 1,000 fold from 1909-1999.\n\nEPA, DHA, ALA\n\nCommon sources: breast milk...\n\nMaintain fluidity of cell membrane and stabilize blood glucose. Also play key role in making anti-inflammatory signals. \n
  • Talk about how to use them!!\n\nEPA v. DHA: EPA probably better. \n\nRecent 2009 meta-analysis published in Journal of American College of Nutrition, looking at more than 200 studies of EPA/DHA found that EPA was associated with improvements in depression. \n\nRecommend minimum of 2 grams 3x/day. That’s 6 grams per DAY. \n\nDemonstration of 6 grams of Omega-3 oil v. 6 grams of Omega-3 capsules. \n
  • The countries that had the lowest fish consumption had highest rates of depression; the countries with highest, had lowest rates of depression. \n
  • Variations on a theme: either blocking a reuptake pump or inhibiting a breakdown enzyme. \n\n\n
  • Key Points:\n\nMAO Inhibitor: Prevents the breakdown of serotonin to 5-HIAA\n\nSerotonin/Norepinephrine reuptake pump: More 5-HT and NE\n\n\nCOMT inhbition is used in Parkinson’s medications. Theoretical target for depression. COMT would spare SAMe\n
  • Donor of methyl groups.\n\nIn my opinion one of the best alternatives to prescription antidepressants. In my practice I have had patients feel better after a few days. \n\nWidely studied, as the next slide shows. \n\nSide effects: GI upset, manic activation\n\nHow I use SAMe: 200 mg in the morning for three days, then 200 mg twice daily; then 400 mg in AM and 200 mg at Noon. Watch for insomnia and mania. Nausea most common side effect. Take with folate. \n
  • Folic acid, vitamin b9, essential cofactor in man biological reactions. \n\nDeficiency associated with neural tube defects like Spina Bifida. \n\nSince 1998, it has been added to cold cereals, flour, breads, pasta, bakery items, cookies, and crackers, as required by federal law.\n\nFolate in diet needs to be converted to L-methylfolate in order to enter brain. Works in concert with SAMe in synthesis of neurotransmitters. \n\nDEMO: Deplin, L-methylfolate.15 mg in am. Onset: weeks. \n
  • Hypericum Perforatum\n\nA report[6] from the Cochrane Review states:\nThe available evidence suggests that the Hypericum extracts tested in the included trials a) are superior to placebo in patients with major depression; b) are similarly effective as standard antidepressants; and c) have fewer side-effects than standard antidepressants.There are two issues that complicate the interpretation of our findings:\n1) While the influence of precision on study results in placebo-controlled trials is less pronounced in this updated version of our review compared to the previous version results from more precise trials still show smaller effects over placebo than less precise trials.\n2) Results from German-language countries are considerably more favorable for hypericum than trials from other countries.\n\nAn analysis of twenty-nine clinical trials with more than five thousand patients was conducted by Cochrane Collaboration. The review concluded that extracts of St John's wort were superior to placebo in patients with major depression. St John's wort had similar efficacy to standard antidepressants. The rate of side-effects was half that of newer SSRI antidepressants and one-fifth that of older tricyclic antidepressants.[6]\n\nMost studies of St John's wort for treating depression used doses of 300 mg of an extract (standardized to 0.3 percent hypericin content) three times daily to achieve a therapeutic effect. Studies suggest to take from 300mg to 1,800 mg daily. There have not been any reports of overdose.[14][15]\n\n Traditional medicine has also employed lipophilic extracts from St John's wort as a topical remedy for wounds, abrasions, burns, and muscle pain.[17] \n\nThe positive effects that have been observed are generally attributed to hyperforin due to its possible antibacterial and anti-inflammatory effects.[17] For this reason hyperforin may be useful in the treatment of infected wounds and inflammatory skin diseases.[17]\n\nThere are side effects that need to be kept in mind. \nMay cause:\n\nDrug drug interactions (may inhibit enzyme that metabolizes Xanax) \nPhotosensitivity \nSerotonin syndrome\n
  • Summarize Key Points of Section:\n\n1) Inflammation is common denominator among many diseases chronic diseases including depression and alzheimer’s\n\n2) Chronic stress leads to chronic inflammation; consequences include physical changes in brain and accelerated aging. \n\n3) Anti-inflammatories, including antidepressants and fish oil, have neuroprotective effect. \n
  • Mr. and Mrs. Hughes, couple in their 70’s. Lived together in assisted living facility in South Bay.\n\nMr. Hughes brought his wife in for behavioral problems associated with her dementia. Screaming and yelling when he was not with her. She was gaining weight at an incredible pace, so much so that she was developing severe arthritis in both knees. \n\nMrs. Hughes also had an eating problem. She could not resist sweets, cookies and candies, that were freely accessible to all residents. \n\nI started her on Aricept and Namenda. She improved but she still had problems fighting with caregivers who had to restrain her from eating sweets or stealing food from other residents.\n\nStarted her on medical food product, Axona, a drink consisting of medium chain triglycerides. Axona is a food product that is approved for treatment of dementia. Glucose is first choice of energy for brain cells, but medium chain triglyerides can also be used. \n\nAfter about a month, she was able to sit with her husband at dinner and she was no longer fighting caregivers for access to sweets. \n\n\n\n\n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • Humans, H. Sapiens, have spent more that 99.5 % of 200,000 year history as hunter-gatherers.\n
  • Humans, H. Sapiens, have spent more that 99.5 % of 200,000 year history as hunter-gatherers.\n
  • Humans, H. Sapiens, have spent more that 99.5 % of 200,000 year history as hunter-gatherers.\n
  • Battle that is not played out in brain; brain receives signals from other parts of the body. \n\nInsulin: allow glucose to enter cells; storage hormone. Insulin causes cells in the liver, muscle, and fat tissue to take up glucose from the blood, storing it as glycogen in the liver and muscle.\n\nLeptin: (greek: Leptos, meaning thin) signals fullness. Produced by adipose cells. Leptin circulates at levels proportional to body fat. Leptin reduced by sleep deprivation; decreases by exercise training. Structurally related to pro-inflammatory cytokine, IL-6, as a response mechanism to prevent cellular stress caused by overeating. Obese individuals exhibit high circulating leptin levels: suggesing leptin resistance. \n\nGrehlin: stimulates appetite. levels increase before meals and decrease after meals; growth hormone releasing; elevated also during chronic stress; lack of sleep also increases grehlin. Gastric bypass lowers grehlin. \n
  • Grehlin goes up\nLeptin goes down\nInsulin goes down\n\nDutch Famine took place in the German-occupied part of the Netherlands, especially in the densely populated western provinces above the great rivers, during the winter of 1944-1945, near the end of World War II. A German blockade cut off food and fuel shipments from farm areas to punish the reluctance of the Dutch to aid the Nazi war effort. Some 4.5 millions were affected and survived because of soup kitchens. About 18,000 died due to the famine\n\nMany adults who were conceived of Dutch famine of 1944 went on to develop chronic disease in adult life, including obesity and depression. There is a higher incidence of schizophrenia in these individuals. \n
  • Grehlin goes up\nLeptin goes down\nInsulin goes down\n\nDutch Famine took place in the German-occupied part of the Netherlands, especially in the densely populated western provinces above the great rivers, during the winter of 1944-1945, near the end of World War II. A German blockade cut off food and fuel shipments from farm areas to punish the reluctance of the Dutch to aid the Nazi war effort. Some 4.5 millions were affected and survived because of soup kitchens. About 18,000 died due to the famine\n\nMany adults who were conceived of Dutch famine of 1944 went on to develop chronic disease in adult life, including obesity and depression. There is a higher incidence of schizophrenia in these individuals. \n
  • Grehlin goes up\nLeptin goes down\nInsulin goes down\n\nDutch Famine took place in the German-occupied part of the Netherlands, especially in the densely populated western provinces above the great rivers, during the winter of 1944-1945, near the end of World War II. A German blockade cut off food and fuel shipments from farm areas to punish the reluctance of the Dutch to aid the Nazi war effort. Some 4.5 millions were affected and survived because of soup kitchens. About 18,000 died due to the famine\n\nMany adults who were conceived of Dutch famine of 1944 went on to develop chronic disease in adult life, including obesity and depression. There is a higher incidence of schizophrenia in these individuals. \n
  • \n
  • Example of a good stress. \n\nDuring short term fast, pro-inflammatory markers go down. \n\nSIRT is a gene that helps promote survival by protecting cells during times when food is scarce. Acts as rescue gene repairing damage done by free radicals. \n\nAlternate-day Diet: Up day: NL caloric intake; down day only 20% of usual calories. Dr. Johnson: volunteers lost 8% of bw in 8 weeks. Reduction in inflammatory markers )(TNF-alpha reduced by 2/3) and improvements in chronic inflammatory conditions like asthma, RA, and HTN. \n\nIntermittent fasting: Confining eating to feeding windows: typically between 3-5 hours/day. \n\nApril 2007 issue of Annals of Nutrition and Metabolism looked at fasting ceremony of Ramadan. Refrain from eating and drinking during daylight hours for 1 month. Looked at 40 healthy, normal weight men and women between 20-39. Showed significant reductions in IL-6, c-reactive protein and homocysteine. IL6 and CRP lasted for 20 days beyond the fasting period. \n
  • Tryptophan depletion in healthy subjects: mixed results, except for those with short version of serotonin transporter gene promotor polymorphism. Study showed subjects with the short allele of the 5-HTTLPR at increased risk to develop depressive symptoms during tryptophan depletion. \n\nDifferent results in patients previously depressed who had responded to SSRIs. \n\nTryptophan depletion: \n\nAlpha-methyl-para-tyrosine: Inhibits tyrosine hydroxylase. \n
  • L-tryptophan competes with leucine, isoleucine valine and tyrosine. Large Neutral Amino Acid Transporter. \n1989 removed from market after some people developed severe muscle and joint pain, fever, weakness. Found to have high levels of white blood cells known as eosinophils. EMS syndrome. 1500 cases reported in us. More than 50 have died. FDA asked manufacturers to voluntarily recall. \nCDC found that EMS could be traced to batches of L-tryptophan produced by a single manufacturer in Japan, which supplied 50-60% of all L-tryptophan in US. \n
  • Feingold diet: Hyperactivity can be triggered by synthetic food colors and flavors and aspartame. \n\nDiets that alter macronturients may have positive impact on mood:\n\nZone diet: 40/30/30; reduces arachadonic acid and omega 3s increase DA/5-HT No studies in depression but effects likely due to reducing carbohydrate load and stabilizing blood sugar. \n\nKetogenic: High fat, adequate protein, low carb diet used to control intractable epilepsy in children. \n\n
  • Forces body to burn fats rather than carbohydrates for energy. Normally, the carbohydrates contained in food are converted into glucose, which is then transported around the body and is particularly important in fueling brain function. However, if there is very little carbohydrate in the diet, the liver converts fat into fatty acids and ketone bodies. The ketone bodies pass into the brain and replace glucose as an energy source\n\nMania and bipolar illness responsive to anti-epileptic drugs: valproate, carbamazepine. Mania also associated with reduction in glucose utilization. \n
  • Most dietary fat is made of molecules called long-chain triglycerides (LCTs). However, medium-chain triglycerides (MCTs)—made from fatty acids with shorter carbon chains than LCTs—are more ketogenic. A variant of the classic diet known as the MCT ketogenic diet uses a form of coconut oil, which is rich in MCTs, to provide around half the calories. As less overall fat is needed in this variant of the diet, a greater proportion of carbohydrate and protein can be consumed, allowing a greater variety of food choices. \n\n\nDEMO: MCTs\n
  • \n
  • \nCase Study: Evelyn is a 58 y.o F with a long hx of schizoaffective disorder. She is conserved and lives with 24 hour live in caregiver. \n\nIn her teen age years she would run away from her parents estate near Palo Alto and go to SF or Oakland to smoke crack cocaine. \n\nIn the 70’s she made suicide attempts by jumping from overpass onto highway 101. \n\nHer problem now was that she was non-compliant with her antipsychotic drug Abilify, and that over the last 10 years she had developed metabolic syndrome as a result of her medications and addiction to sugar. \n\nWhenever her caregivers weren’t looking she would go through the kitchen looking for chocolate. Things got so bad that caregivers had to lock her refrigerator and cabinets. \n\nWhen I asked her what her addiction was like, she said that her addiction to sugar was a little like her addiction to crack cocaine. \n\n
  • Historically, our consumption of sugar has increased over the last century. \n\nHistorically, we ate the equivalent of only 20 teaspoons of sugar a year as a hunter/gatherer species. Now we consume about 50 teaspoons...a day. That amounts to 158 lbs per person/per year.\n\nIn the U.S. we have become addicted to sugar. Robert Lustig, obesity research out of UCSF, in February 2012 Nature opinion piece, argues we should control consumption like alcohol.\n\nType 2 diabetics have four times the risk of getting Alzheimer’s. \n\nWe evolved to keep the levels of glucose under tight control because glucose is primary fuel source of brain and muscle. Generally, our brains like to have blood glucose of at least 70 mg/DL.\n
  • \nWhen blood sugar is low, this is registered by insulin receptor in hypothalamus. This, in turn, results in a number of symptoms including emotional lability (amydala) and impaired judgment (frontal cortex). \n\nWhen blood glucose goes even lower, to about 55, this activates the HPA stress axis, epinephrine and cortisol released, and excessive HPA stimulation result. Prolonged hypoglycemia impairs cognitive function and motor control. \n\n\n\n
  • On the opposite side of the coin, we have hyperglycemia, define as blood glucose of greater than 200. Hyperglycemia symptoms include frequent urination, blurred vision and coma. Insulin levels rise abruptly, and over time insulin levels become chronically elevated. \n\nOver time, cells become less responsive to insulin, the storage hormone, and glucose levels remain elevated instead of being stored in cells and used for energy. At first this excess glucose gets broken down and converted to triglycerides. With even more time, this excess glucose sticks to the surface of cells and causes AGEs: advanced glycation end products. This AGEs trigger inflammation. This can be measured on the surface of red blood cells by checking Hemoglobin A1C, which gives clinicians a rough idea of glycemic control over the last 4 months. This results in condition of prediabetes, defined clinically as fasting bloood glucose of 100-125. \n\nAs an aside, many of the drugs we use to treat psychosis can cause metabolic syndrome (BMI > 28, elevated fasting blood glucose, and waist circumference >40, elevated triglycerides, low HDL, high blood pressure). Usually a predictable sequence of events: elevated blood glucose, elevated triglycerides, then elevated hemoglobin A1C. Elevated triglycerides may be the earliest predictor than someone is going to develop metabolic syndrome or diabetes. \n\nAlong this pathway, insulin secretion is exaggerated sometimes, and overshoots in anticipation of another high glucose load; this in turn can sometimes cause hypoglycemia. Evidence that this system is tightly regulated and gauged by previous experience. It has been noted that some foods cause a sharper rise in blood glucose, and therefore insulin, compared to others with the same nutrients. \n\nBrain, like muscle, will preserve glucose. Muscles will replenish glucose after exercise; a similar phenonemon is seen in astrocytes (specialized brain cell) after exercise: they supercompensate after a single bout of exercise. Brain cell carbo load. Brain cells that supercompensate the most: in frontal cortex and hippocampus. \n\nTake home point: keep your blood sugar stable by consuming smaller meals ever 3-4 hours. Don’t wait until you’re hungry. \n\nWhat else should you do? Eat foods that have a low glycemic index. \n
  • The glycemic index is a measure of how much and how quickly a food will raise blood glucose. \n\nSucrose is the standard of measure. Sucrose has a GI of 100. Just to put this in perspective, food with the highest GI include high fructose corn syrup with a GI of . Among foods with the lowest GI are....\n\nThe high glycemic foods include refined grains, potatoes and sugary foods. These are foods that may lead to an over-exaggerated insulin response. \n\nLow GI foods include whole grains, legumes, and some fruit. \n\nBlood glucose can be stabilized by emphasizing low GI foods and eating smaller, more frequent meals. \n\nMy favorite in between meal snack: \n\n10-15 whole almonds\n1 glass of coconut milk with chocolate protein powder. \n\n\n
  • \nHow many grams of fiber is recommended in American diet? 30 grams/day\n\nHow many grams of fiber do we actually get? Less than 15 grams. \n\nIs it any wonder then that with consumption of 50+ teaspoons of sugar and less than 50% of RDA of fiber that there is an obesity epidemic in America? \n\nSo what is fiber exactly?\n\nFiber is group of undigestable group of compounds, found in food, that cannot be digested. \nThere are different forms, including psyllium, glucommann, polyclyccoplex and Konjac root.\n\nDEMO: Psyllium fiber v. Polyglycoplex\n\nFiber has the net effect of stabilizing blood sugar by slowing rate of absorption from the small interesting. Some forms of fiber also promote healthy bacterial flora in the gut...probiotics, of sorts.\n\nMany controlled studies clearly demonstrate the the blood glucose stabilizing effects of fiber. Here’s one from....that shows the effect of psyllium and blood glucose. \n
  • Background: Water-soluble dietary fibers decrease postprandial glucose concentrations and decrease serum cholesterol concentrations. This study examined the effects of administering psyllium to men with type 2 diabetes.\n\nObjective: The objective was to evaluate the safety and effectiveness of psyllium husk fiber used adjunctively to a traditional diet for diabetes in the treatment of men with type 2 diabetes and mild-to-moderate hypercholesterolemia.\n\nDesign: After a 2-wk dietary stabilization phase, 34 men with type 2 diabetes and mild-to-moderate hypercholesterolemia were randomly assigned to receive 5.1 g psyllium or cellulose placebo twice daily for 8 wk. Serum lipid and glycemic indexes were evaluated biweekly on an outpatient basis and at weeks 0 and 8 in a metabolic ward.\n\nResults: In the metabolic ward, the psyllium group showed significant improvements in glucose and lipid values compared with the placebo group. Serum total and LDL-cholesterol concentrations were 8.9% (P < 0.05) and 13.0% (P = 0.07) lower, respectively, in the psyllium than in the placebo group. All-day and postlunch postprandial glucose concentrations were 11.0% (P < 0.05) and 19.2% (P < 0.01) lower in the psyllium than in the placebo group. Both products were well tolerated, with no serious adverse events related to treatment reported in either group.\n\nConclusion: The addition of psyllium to a traditional diet for persons with diabetes is safe, is well tolerated, and improves glycemic and lipid control in men with type 2 diabetes and\nhypercholesterolemia. Am J Clin Nutr 1999;70:466–73\n
  • Let’s review a few points about glucose and the brain that I’ve already mentioned.\n\nWe remember that the brain uses about 25% of the glucose that is available to the body. This is all the more remarkable when you remember that the brain only takes up about 2% of body weight. \n\nWhen blood glucose levels fall to low because of low intake or metabolic abnormalities, this is registered in both primitive brain and more evolved prefrontal cortex. We become irritable, impatient, or aggressive. Any of us who have been on diets have experienced this. \n\nIn the brain we have at least two pathways, one primitive, one more evolved, but when push comes to shove, the reptilian brain will almost always win. Why? Because the components that are so much a part of modern diet--Sugar, fat , and salt activate the reward circuits (mesolimbic dopamine) that govern self-control. Primitive circuits will always win. \n\nThis is why diets don’t work. You can’t will yourself out of eating any more than a crack addict can will away desire for cocaine. \n
  • Let’s review a few points about glucose and the brain that I’ve already mentioned.\n\nWe remember that the brain uses about 25% of the glucose that is available to the body. This is all the more remarkable when you remember that the brain only takes up about 2% of body weight. \n\nWhen blood glucose levels fall to low because of low intake or metabolic abnormalities, this is registered in both primitive brain and more evolved prefrontal cortex. We become irritable, impatient, or aggressive. Any of us who have been on diets have experienced this. \n\nIn the brain we have at least two pathways, one primitive, one more evolved, but when push comes to shove, the reptilian brain will almost always win. Why? Because the components that are so much a part of modern diet--Sugar, fat , and salt activate the reward circuits (mesolimbic dopamine) that govern self-control. Primitive circuits will always win. \n\nThis is why diets don’t work. You can’t will yourself out of eating any more than a crack addict can will away desire for cocaine. \n
  • Let’s review a few points about glucose and the brain that I’ve already mentioned.\n\nWe remember that the brain uses about 25% of the glucose that is available to the body. This is all the more remarkable when you remember that the brain only takes up about 2% of body weight. \n\nWhen blood glucose levels fall to low because of low intake or metabolic abnormalities, this is registered in both primitive brain and more evolved prefrontal cortex. We become irritable, impatient, or aggressive. Any of us who have been on diets have experienced this. \n\nIn the brain we have at least two pathways, one primitive, one more evolved, but when push comes to shove, the reptilian brain will almost always win. Why? Because the components that are so much a part of modern diet--Sugar, fat , and salt activate the reward circuits (mesolimbic dopamine) that govern self-control. Primitive circuits will always win. \n\nThis is why diets don’t work. You can’t will yourself out of eating any more than a crack addict can will away desire for cocaine. \n
  • Let’s review a few points about glucose and the brain that I’ve already mentioned.\n\nWe remember that the brain uses about 25% of the glucose that is available to the body. This is all the more remarkable when you remember that the brain only takes up about 2% of body weight. \n\nWhen blood glucose levels fall to low because of low intake or metabolic abnormalities, this is registered in both primitive brain and more evolved prefrontal cortex. We become irritable, impatient, or aggressive. Any of us who have been on diets have experienced this. \n\nIn the brain we have at least two pathways, one primitive, one more evolved, but when push comes to shove, the reptilian brain will almost always win. Why? Because the components that are so much a part of modern diet--Sugar, fat , and salt activate the reward circuits (mesolimbic dopamine) that govern self-control. Primitive circuits will always win. \n\nThis is why diets don’t work. You can’t will yourself out of eating any more than a crack addict can will away desire for cocaine. \n
  • I’ve already mentioned how glucose and insulin affect the brain. In the previous section I mentioned how other hormones like grehlin and leptin also regulate appetite.\n\nInsulin levels, in response to glucose, secreted by pancreas and registered in hypothalamus\n\nFat cells, we learned, also secret the hormone leptin, which is also registered by hypothalamaus. Take input on computes: Should breakdown, catabolic signals increase, or should anabolic (storage and building processes) take place. Hypothalamus send send these signals to the NTS. \n\nWhen this signalling system becomes dysfunctional, insulin resistance sets, then prediabetes, diabetes set in. This is becoming an epidemic. \n
  • About one in four adults had prediabetes in 2007. Most of thse will go in to develop type 2 diabetes within 10 years. \n\n[Show graph of diabetes development in America. ]\n
  • \n
  • \n
  • Advertisement for Desoxyn 1957: When She Can’t Escape Temptation, Prescribe Dexosyn. \n
  • In response to this, a whole new interest in drugs to suppress appetite. These drugs work at the level of neurotransmitters like DA, NE, but we just learned that regulation of appetite involves a variety of hormonal inputs, not just altering neurotransmitters. Morever, the same neurotrasmitter has different functions depending on what part of the brain its working on. NE in the lateral hypothalamus will....But increase NE levels in the ....and appetite will increase. It’s not surprising that most studies of weight loss agents have been modest. Meta-analysis have shown that the average placebo-subtracted weight loss to be 3-5%. \n\nHere is just a rundown of these drugs:\n\nDrugs like psychostimulant to supress appetite. They have been available since 1947. Do you know what the first commercially available drug for suppressing appetite was? It was Desoxyn...short for desoxyephedrine. Do you know the other name for desoxyephedrine? methamphetamine. Do I use methamphetamine in my practice? Yes. \n\nShow an add for desoxyn? \n\nPhentermine, half of the Phen/Fen combo, is still available. Fenfluramine was discontinued in 1997due to concerns about primary pulmonary hypertension and cardiac fibrosis. According to a study of almost 6,000 former users, damage to heart valves was noted in 20% of women and 12% of men. For a while, after fenfluramine was withdrawn, Prozac was substituted, Phen/Pro, but combo was not as effective. \n\nSibutramine is a reuptake inhibitor (no longer available in US due to concerns about stroke). Makers of the drug (abbott) withdraw the drug from the market under pressure from the FDA about concerns with adverse CV events. The preliminary data shows that cardiovascular events were reported in 11.4% of patients using sibutramine compared to 10% of patients using a placebo. I believe it was withdrawn prematurely because of the phentermine scare. \n\nIf you use a research tool like google scholar and you search for “appetite suppressant” you get a spate of articles about primary pulmonary hypertension. \n\nMore recently, combination medications are under development.\n\nAmong the more recent are Contrave, which is a combination of the NE antidepressant bupropion and naltrexone, an opiod receptor antagonist. \n\nThere is also Empatic, a zonisamide/bupropion combination under development. Zonisamide is a anticonvulsant medication. \n\nOrlistat, the fat blocking medication, is the only drug that is currently approved for long-term management of obesity. Major side effect: steatorrhea. The last thing you want to do is get on a MCT diet on orlistat at same time. \n\nAlong the line of natural appetite suppressant, I think I’d put psyllium at the top of my list. Key is to control blood sugar and hormones, not neurotransmitters. As a psychopharmacologist I think best option is not to go there with natural stimulants. \n\nNevertheless, here’s my list of natural appetite suppressants:\n\nCaffeine\nCinnamon\nAlmonds\n
  • \n
  • Branched chain amino acids include leucine, isoleucine, and valine. They are all essential amino acids and the body can convert them to glucose if needed. \n\nThey are recognized to have medical uses, including the treatment of tardive dyskinesia.\n\nThey have been shown to improve exercise performance , attenuate the stress hormone response to exercise and reduce DOMS. BCAAs lower the cortisol level often seen with intense and prolonged exercise. Amino Acid supplements and recovery from high-intensity resistance training)\n\nDEMO: Branch Chain Aminos mixed in Diet Cranberry Juice. \n\nThey also help stabilize blood sugar. The next slide shows how.\n
  • The three key players of glucose load are muscle, liver, and influx from intestine. \n\nMuscle \n\n“Because muscle mass determines 40% of an individual’s ability to handle insulin and approximately 80% of a person’s blood sugar use , muscle is perhaps one of the most valuable resource in weight loss protocols”\n\nThese aminos generate the gluconeogenic precursors glutamine and alanine, which has an effect on stability blood sugar.\n\nGlutamine is a conditionally essential amino acid. Useful in treatment of injuries, trauma, burns. I saw it used in pharmacology lab: media for cell culture. I also saw it used in ER in King-Drew Medical Center for trauma. 90% of glutamine in body is in muscle mass. Study found that 2 grams of glutamine were enough to raise human growth hormone, the manna of the anti-aging and body building community. \n\nAlanine is an essential amino acid. It travels from muscle to liver where it can get converted to glucose. Do you see how clever this is? Alanine does not raise insulin! \n\nFebruary 2011 population study out of Journal of Nutrition looked at a cohort of 4, 425 subjects from Japan, USA and China. Positive correlation for escalating intake of BCAA and reduced risk of being overweight or obese. \n\nFinally, pilot study out of journal AGE showed a dose of 12 g BCAA in combination with DHA resulted in a 4 lb weight loss within two weeks in women over age 38. “Nutrient signalling system using Leucine and DHA”. \n \nNow that’s a pretty potent combination strategy!\n\nConclusion:\n\nControl blood sugar with:\nMore frequent meals with low glycemic index\nIncrease fiber intake to 30 g/day\nBCAAs or Glutamine\n\n\n
  • The three key players of glucose load are muscle, liver, and influx from intestine. \n\nMuscle \n\n“Because muscle mass determines 40% of an individual’s ability to handle insulin and approximately 80% of a person’s blood sugar use , muscle is perhaps one of the most valuable resource in weight loss protocols”\n\nThese aminos generate the gluconeogenic precursors glutamine and alanine, which has an effect on stability blood sugar.\n\nGlutamine is a conditionally essential amino acid. Useful in treatment of injuries, trauma, burns. I saw it used in pharmacology lab: media for cell culture. I also saw it used in ER in King-Drew Medical Center for trauma. 90% of glutamine in body is in muscle mass. Study found that 2 grams of glutamine were enough to raise human growth hormone, the manna of the anti-aging and body building community. \n\nAlanine is an essential amino acid. It travels from muscle to liver where it can get converted to glucose. Do you see how clever this is? Alanine does not raise insulin! \n\nFebruary 2011 population study out of Journal of Nutrition looked at a cohort of 4, 425 subjects from Japan, USA and China. Positive correlation for escalating intake of BCAA and reduced risk of being overweight or obese. \n\nFinally, pilot study out of journal AGE showed a dose of 12 g BCAA in combination with DHA resulted in a 4 lb weight loss within two weeks in women over age 38. “Nutrient signalling system using Leucine and DHA”. \n \nNow that’s a pretty potent combination strategy!\n\nConclusion:\n\nControl blood sugar with:\nMore frequent meals with low glycemic index\nIncrease fiber intake to 30 g/day\nBCAAs or Glutamine\n\n\n
  • The three key players of glucose load are muscle, liver, and influx from intestine. \n\nMuscle \n\n“Because muscle mass determines 40% of an individual’s ability to handle insulin and approximately 80% of a person’s blood sugar use , muscle is perhaps one of the most valuable resource in weight loss protocols”\n\nThese aminos generate the gluconeogenic precursors glutamine and alanine, which has an effect on stability blood sugar.\n\nGlutamine is a conditionally essential amino acid. Useful in treatment of injuries, trauma, burns. I saw it used in pharmacology lab: media for cell culture. I also saw it used in ER in King-Drew Medical Center for trauma. 90% of glutamine in body is in muscle mass. Study found that 2 grams of glutamine were enough to raise human growth hormone, the manna of the anti-aging and body building community. \n\nAlanine is an essential amino acid. It travels from muscle to liver where it can get converted to glucose. Do you see how clever this is? Alanine does not raise insulin! \n\nFebruary 2011 population study out of Journal of Nutrition looked at a cohort of 4, 425 subjects from Japan, USA and China. Positive correlation for escalating intake of BCAA and reduced risk of being overweight or obese. \n\nFinally, pilot study out of journal AGE showed a dose of 12 g BCAA in combination with DHA resulted in a 4 lb weight loss within two weeks in women over age 38. “Nutrient signalling system using Leucine and DHA”. \n \nNow that’s a pretty potent combination strategy!\n\nConclusion:\n\nControl blood sugar with:\nMore frequent meals with low glycemic index\nIncrease fiber intake to 30 g/day\nBCAAs or Glutamine\n\n\n
  • Case Study: Noel Beauchamp\n\nIn this section, we will talk about nutrients to improve attention/ awareness and discuss practical strategies for optimizing sleep. \n
  • There is a epidemic of inattention in US. Distracted by technology that is supposed to make our lives easier: cell phones, internet. My daughters triple screening: she sitting on the living room couch, had cell phone by her side, working on her lap top (probably face booking), while the TV was on. \n\nADD has become shorthand for “being distracted”. \n\nEdward Hallowell, author of driven to distraction, has identified syndrome he calls attention-deficit trait, subsyndromal ADD. \n\nADD is defined as problem regulating attention. Affects as many as 20% of school-aged children about 5% of american adults. Criteria are changing for making diagnosis in children, and there are NO criteria for diagnosing adults. \n\nCriteria include the following three symptom clusters: Inattention, impulsivity, and hyperactivity.\nAnd the symptoms are severe enough to cause dysfunction in least two different areas. Criteria are being revised; it is now recognized as spectrum disorder. \n\nAs the criteria are revised, it will be interesting to see if the criteria catch more adults, but I think it’s fair to say that most of us suffer from attention deficit traits.\n\nFrom biologic standpoint, ADD is thought to be caused by dysregulation of NE in frontal cortex. First line treatment is use of psychostimulants: Ritalin, Adderall, or Dextroamphetamine: drugs that increase NE transmission in frontal cortex. \n
  • Nutrients, as we have already learned, can also have a profound impact on improving attention and concentration. \n\nHere is a list of the most common nutrients I use in my practice. (Added B-Vitamins) \n\nSAMe is a methyl donor that is important in synthesis of neurotransmitters. \n\nB-vitamins, folate and B12, are important in synthesis of neurotransmitters and their turnover. \n\nOmega-3 fatty acids stabilize cell membranes and receptors; help neurotransmitters function better. \n\nL-tyrosine: a precursor of the amino acid dopamine. Remember the L-tyrosine is converted via tyrosine hydroxylase, to dopamine. \n\nFinally,: Dimethylamino ethanol, which is a precursor for the synthesis of acetylcholine. It is believed to be methylated to produce choline in the brain. Studies have shown an increase in alertness and positive influence on mood. The dose I recommend for patients is 100 mg 3x/day\n\nI just wanted to spend a few more moments with what I think is probably most underutilzed and readily available formulation to treat ADHD: B-Vitamins. \n
  • Stress depletes the bodies stores of b-vitamins. \n\nAntidepressants are also believed to increase b-vitamin turnovers. \n\nLab tests: B-12/Folic Acid/Homocysteine levels \n\nIn any of the OTC formulations, including energy drinks, they are key ingredient, along with caffeine. For my patients I recommend that they take a balanced B -complex in the morning with food. The most common side effect is nausea. \n\n[I thought I would say a little more about caffeine. It works primarily as a CNS stimulant. It readily crosses BB barrier and actually works by antagonizing adenosine receptors. In brain, high levels of adenosine induce sleep. ]\n\nWhen thinking about inattention, I thinks it’s important to consider other coexsiting conditions that can also impair attention. In fact, more than 60% of adults with ADHD also have a coexisting anxiety disorder, which can also impair attention.\n
  • It’s estimated that about 2 in 5 American suffer from a form of anxiety. Only about 1/3 of those with anxiety are receiving treatment. The most common disorders are:\n\nGAD with a prevalence of 3%\nPD with a prevalence of 2.7%\nPTSD with a prevalence of 3.5%\nand OCD with a prevalence of 1%\n\nSome of the dietary supplements to treat anxiety disorder are listed here. \n\nIs incidence of obesity higher in anxiety disorder than in depressive disorders? \n
  • What is most common way to treat anxiety? Alcohol. Alcohol works on GABA receptor, but so do many of the substances listed here. \n\nI’ll talk more about two of these (Kava and Valerian) , but I’d just point out that almost all of them are thought to work on GABA, the primary inhibitory neurotransmitter in CNS. \n\nL-theanine is an amino acid derivative. It’s found in green tea. It’s also available as a topical skin cream. Thought to inhibit glutamate excitotoxicty. Structurally realted to glutamate. \n\nGABA supplements, by the way, are not GABA in a pill. They do not cross BB barrier. They do have mild peripheral actions. I rarely recommend them. \n\n\nKava has an interesting history. Used widely in polynesian cultures. Active ingredient are Kava Lactones. Pill contains about 60 to 150 kavalactones, but traditionally prepared beverage has about 250 kava lactones.\n\nValerian is very popular as sedative, especially among U.S. Hispanics. Typical doses of about 2-10 grams/day. Used most often for insomnia. One of components, valeric acid, is analogue of valproic acid, the anticonvulsant drug. Also a cat attractant similar to catnip. Odor mimics cat urine. Also attracts rats. Pied Piper of Hamelin used his pipes and Valerian to attract rats. \n
  • \n
  • \n
  • When we turn to treatment of more specific anxiety disorders, NAC, or n-acetylcysteine is one of more interesting compounds. Amino acid derivative of cysteine. \n\nWides recognized as anti-oxidant. \n\nInteresting and emerging literature in use of OCD and impulse control disorders. \n\nBelieved to stabilize glutamate level, especially in associated with impulse control eating. \n\n600 mg 3x/day; last dose no later than 5 hours before bedtime. \n
  • I think it’s important to mention in passing the vital role of magnesium. (almonds, spinach)\n\nMost important role is that it helps improve insulin resistance and glucose utilization.\n\nAvoid magnesium oxide or magnesium carbonate; for adults RDA is 420/320. Magnesium sulfate/chloride/lacate or citrate have better bioavailability. \n\nDEMO: Magnesium Lactate formulation from GNC. \n\n\n\n\n
  • When we consider nutrients for enhancing cognitive performance, many of the same players arise: Omega, B-vitamins, and MCTs (Axona) \n\nA couple I haven’t mentioned are Ginko Biloba and PC. \n
  • Ginko is a plant. Ginkgo is believed to have nootropic properties, and is mainly used as memory and concentration enhancer. \n\nMixed results in studies for dementia. Doses are 120-240 mg/day. \n\nI have not seen any significant improvements in my patients. \n
  • PC/PS: major component of cell membranes. Found in egg yolk and soy beans. Member of lecithin (greek for egg yolk) group of fats. FDA concludes that PC not help for dementia.\n\nWith PS, FDA concluded that it may reduce the risk of dementia in the elderly.\n\nPS also shown to speed up recovery and prevent muscle soreness. Doses of 400 mg may reduce exercise-induced cortisol levels. \n
  • \nCocoa and chocolate have recently been found to be rich plant-derived sources of antioxidant flavonoids with beneficial cardiovascular properties. These favorable physiological effects include: antioxidant activity, vasodilation and blood pressure reduction, inhibition of platelet activity, and decreased inflammation. Increasing evidence from experimental and clinical studies using cocoa-derived products and chocolate suggest an important role for these high-flavanol-containing foods in heart and vascular protection.\n\n\nEvidence based on epidemiological studies suggests\nthat flavonoid-rich diets high in fruits and/or vegetables reduce the risk of coronary heart disease.\n\nRecent studies also report reduced cardiovascular risk and events associated with the consumption of foods rich in\nflavonoids.\n\nA meta-analysis of seven prospective cohort studies with 105,000 individuals indicates that highdietary intake of flavonoids from a small number of fruits\nand vegetables, tea, and red wine is inversely associated with coronary heart disease risk\n\nDietary flavonoids and their potential role in the prevention of cardiovasculardisease have gained recent scientific and medical interest\ndue to their antioxidant properties: their ability to scavenge reactive oxygen species (ROS) and reactive nitrogen species.\n7,\n
  • 1. Nurk E, Refsum H, Drevon CA, et al. Intake of flavonoid-rich wine, tea, and chocolate by elderly men and women is associated with better cognitive test performance. The Journal of Nutrition. 2009;139(1):120.\n\nAbstract\nIn a cross-sectional study, we examined the relation between intake of 3 common foodstuffs that contain flavonoids (chocolate, wine, and tea) and cognitive performance. 2031 participants (70–74 y, 55% women) recruited from the population-based Hordaland Health Study in Norway underwent cognitive testing. A cognitive test battery included the Kendrick Object Learning Test, Trail Making Test, part A (TMT-A), modified versions of the Digit Symbol Test, Block Design, Mini-Mental State Examination, and Controlled Oral Word Association Test. Poor cognitive performance was defined as a score in the highest decile for the TMT-A and in the lowest decile for all other tests. A self-reported FFQ was used to assess habitual food intake. Participants who consumed chocolate, wine, or tea had significantly better mean test scores and lower prevalence of poor cognitive performance than those who did not. Participants who consumed all 3 studied items had the best test scores and the lowest risks for poor test performance. The associations between intake of these foodstuffs and cognition were dose dependent, with maximum effect at intakes of ;10 g/d for chocolate and ;75– 100 mL/d for wine, but approximately linear for tea. Most cognitive functions tested were influenced by intake of these 3 foodstuffs. The effect was most pronounced for wine and modestly weaker for chocolate intake. Thus, in the elderly, a diet high in some flavonoid-rich foods is associated with better performance in several cognitive abilities in a dose-dependent manner. J. Nutr. 139: 120–127, 2009.\n\n
  • This is an info graphic that summarizes a lot of information about supplements. \n\nOne’s to watch: Cocoa (because of PEA?) and NAC. \n\nFolic acid and fish oil: no suprise there.\n\nFor the interactive graphic go to informationisbeautiful.net. \n
  • On average we get 6.5 hours of sleep/night. Optimal functioning requires 8. \n\nMoreover, about 1/3 of US adults experience frequent difficulties with sleep initiation. \n\nWhat are the consequences of this? \n\nSleep Disorders: Production of pro inflammatory cytokines TNF alpa appears to follow a circadian rhythm. Disruption of normal sleep can lead to daytime elevations of these pro-inflammatory molecules. Plasma levels of TNF-α and/or IL-6 were elevated in patients with excessive daytime sleepiness, including those with sleep apnea and narcolepsy\nSleep deprivation is associated with increase in food consumption and appetite. \n\nA recent study published in 2012, shows that a specific brain region that contributes to a person’s appetite sensation is more activated in response to food images after one night of sleep loss than after one night of normal sleep.\n\nIt’s been shown that after a single night of partial sleep deprivation, markers of inflammation are increased IL-6 and TNF-alpha and C-reactive protein.\n\nIn a 2006 study, 30 healthy volunteers proinflammatory cytokines were measured during the day across three baseline periods and after partial sleep deprivation (awake from 11 PM to 3 AM) . \n\nIn adults with chronic inflammatory disorders (diabetes, depression, asthma, RA), sleep maintenance is further disturbed. \n\nChronic insomnia increase the risk of depression 5 times, the risk for panic disorder 20x. \n
  • Let’s take a look at a normal sleep architecture. This is a hypnogram. \n\nDiscrete stages: fast wave sleep (stage 1 and 2); slow wave sleep (stage 3 and 4). Cycles throughout the night of about 90-120 minutes. There are about 4-5 sleep cycles each night. REM sleep becomes more common during the latter part of the night. \n\nAs we get older slow wave sleep decreases and light sleep increases. \n\nIndividuals with MDD have changes in sleep architecture:\nShortening of the time from sleep onset to the appearance of the first REM (Short REM latency)\nIncreased REM activity\nChanges in temporal distribution of REM: First REM is longest; last is shortest; opposite of NL\n\nSo to increase our chances of getting a good night’s sleep, we need to practice good sleep hygeine:\n\nMaintain a regular bedtime and arise time\nConform time spent in bed to time necessary for sustained and adequate sleep\nRestrict alcohol and caffeine beverages before bedtime\nEmploy exercise and good nutrition\nControl environmental factors so that they enhance, not disturb restful sleep\n
  • Sleep is controlled by an area in the brain called the suprachiasmatic nucleus, located in the hypothalamus. Its about the size of a grain of rice. This is the area most associated with circadian rhythms. The pacemaker of rhythms. \n\nThis group of neurons sends signals to other parts of the brain to control things like sleep, metabolism, immune system activity, body temperature and hormone production and a schedule slightly longer than 24 hours. \n\nSCN responds to environmental light. When light is detected, SCN neurons send signal to pineal gland, which shuts down endogenous production of melatonin. \n
  • Melatonin plays a major role in the regulation of sleep and other cyclical bodily activities. It is derived from serotonin. \n\nExogenous melatonin has been used for certain types of insomnia. (Delayed sleep phase syndrome) . Meta-analysis in 2006 found no evidence that melatonin was effective in treating insomnia, jet lag or shiftwork sleep disorder. \n\nRecommended doses are 0.25 to 3.0 mg/day. \n
  • The next slide demonstrates how melatonin fluctuates over a 24 hour time period. \n\nThe human body produces its own (endogenous) melatonin starting about two hours before bedtime, provided the lighting is dim. This is known as dim-light melatonin onset, DLMO. This stimulates the phase-advance portion of the PRC and helps keep the body on a regular sleep-wake schedule. It also helps prepare the body for sleep.\n
  • For humans, a treatment designed to affect circadian rhythms will most often be intended to adjust sleep timing, either delaying it to later in the day (night), or advancing it. Extreme morning people may want to delay their sleep timing; extreme evening chronotypes may wish to advance it.\n\nAdvanced sleep phase disorder (ASPD), also known as the advanced sleep-phase type (ASPT) of circadian rhythm sleep disorder or advanced sleep phase syndrome (ASPS), is a condition in which patients feel very sleepy and go to bed early in the evening (e.g. 6:00–8:00 p.m.) and wake up very early in the morning (e.g. around 3:00 a.m.).\n\nDelayed sleep-phase disorder (DSPD), also known as delayed sleep-phase syndrome (DSPS) or delayed sleep-phase type (DSPT), is a circadian rhythm sleep disorder, a chronic disorder of the timing of sleep, peak period of alertness, the core body temperature rhythm, hormonal and other daily rhythms, compared to the general population and relative to societal requirements. People with DSPD generally fall asleep some hours after midnight and have difficulty waking up in the morning.\n\nOften, people with the disorder report that they cannot sleep until early morning, but fall asleep at about the same time every "night". Unless they have another sleep disorder such as sleep apnea in addition to DSPD, patients can sleep well and have a normal need for sleep. Therefore, they find it very difficult to wake up in time for a typical school or work day. If, however, they are allowed to follow their own schedules, e.g. sleeping from 4 a.m. to noon, they sleep soundly, awaken spontaneously, and do not experience excessive daytime sleepiness.\n\n\nBright light therapy has been shown to be effective for seasonal affective disorder. \n\nA meta-analysis by the Cochrane Collaboration concluded that "For patients suffering from non-seasonal depression, light therapy offers modest though promising antidepressive efficacy."[20] A more recent meta-analysis from Journal of Affective Disorders confirms this and is even more hopeful: "Overall, bright light therapy is an excellent candidate for inclusion into the therapeutic inventory available for the treatment of nonseasonal depression today, as adjuvant therapy to antidepressant medication, or eventually as stand-alone treatment for specific subgroups of depressed patients."[21]\n\nLight of 10,000 lux for a minimum of 30 minutes as effective as antidepressants. \n\nBright light therapy, according to study in 2003, was also found to increase LH levels, a hormone that raises testosterone in me. Researchers found that LH levels increased by 70% after bright light therapy. May ease sexual dysfunction in men according to UCSD researchers. \n\nHow to use light therapy? \n\ncet-surveys.org. Morningness-eveningness type. Will give you instructions on when to start light therapy. \n\nTiming is important: Indeed, light therapy given 7.5 to 9.5 hours after melatonin onset yields twice the remission rate (80% versus 38%) of light given 9.5 to 11.0 hours after melatonin onset” \n\nIn a newer study (2006), Victoria L. Revell et al. have shown that a combination of morning bright light and afternoon melatonin, both timed to phase advance according to the respective PRCs, produce a larger phase advance shift than bright light alone,[6] for a total of up to 21⁄2 hours.\n\n
  • \n
  • \n
  • \n
  • \n
  • \n

Food For Thought: How Nutrients Affect the Brain Food For Thought: How Nutrients Affect the Brain Presentation Transcript

  • Food For Thought: HowNutrients Affect The Brain Michael Lara, MD Diplomate, American Board of Psychiatry and Neurology Private Practice Psychiatry and Psychopharmacology Belmont, CA email: mlaramd@yahoo.com Twitter: FlamingBrains Facebook: www.facebook.com/FlamingBrains
  • Program Overview
  • Program Overview• Nutrition and Neurotransmitters
  • Program Overview• Nutrition and Neurotransmitters• Inflammation and Mood
  • Program Overview• Nutrition and Neurotransmitters• Inflammation and Mood• Stress-Related Eating and Appetite
  • Program Overview• Nutrition and Neurotransmitters• Inflammation and Mood• Stress-Related Eating and Appetite• Blood Sugar, Brain and Behavior
  • Program Overview• Nutrition and Neurotransmitters• Inflammation and Mood• Stress-Related Eating and Appetite• Blood Sugar, Brain and Behavior• Optimizing Sleep and Awareness
  • Nutrients that InfluenceKey Neurotransmitters
  • Neurotransmitter Function
  • Neurotransmitter Function• Neurotransmitters are messenger molecules produced by nerve cells to communicate and control almost every function of the body: mood, memory, appetite, and sleep-wake cycle
  • Neurotransmitter Function• Neurotransmitters are messenger molecules produced by nerve cells to communicate and control almost every function of the body: mood, memory, appetite, and sleep-wake cycle• Many are made from essential amino acids from nutrients
  • Neurotransmitter Function• Neurotransmitters are messenger molecules produced by nerve cells to communicate and control almost every function of the body: mood, memory, appetite, and sleep-wake cycle• Many are made from essential amino acids from nutrients• Psychopharmacology focused on mimicking or altering the effects of neurotransmitters
  • Amino Acid Building Blocks
  • Amino Acid Building Blocks• Protein from diet is broken down into amino acids; during starvation muscle protein is broken down
  • Amino Acid Building Blocks• Protein from diet is broken down into amino acids; during starvation muscle protein is broken down• Amino acids are converted, with the help of cofactors, to neurotransmitters in CNS
  • Amino Acid Building Blocks• Protein from diet is broken down into amino acids; during starvation muscle protein is broken down• Amino acids are converted, with the help of cofactors, to neurotransmitters in CNS• Amino acids also are used to make membrane receptors for neurotransmitters
  • Amino Acid Building Blocks• Protein from diet is broken down into amino acids; during starvation muscle protein is broken down• Amino acids are converted, with the help of cofactors, to neurotransmitters in CNS• Amino acids also are used to make membrane receptors for neurotransmitters• The only source of the essential amino acids is the protein in your diet
  • Tryptophan Methionine Phenylalanine Threonine Valine Leucine Isoleucine Lysine Cysteine Tyrosine Glycine Serine Taurine Carnitine Aspartic Acid Glutathione Thyroxine Glutamine Glutamate Asparagine PyroglutamateTryptamine Serotonin Dopamine GABA Melatonin Epinephrine Norepinephrine Essential Amino Acid (must be obtained from diet) Non-essential Amino Acid (made from essential) Neurotransmitter
  • Serotonin
  • Serotonin• Neurotransmitter associated with feelings of well- being and happiness
  • Serotonin• Neurotransmitter associated with feelings of well- being and happiness• Also regulates sleep and appetite
  • Serotonin• Neurotransmitter associated with feelings of well- being and happiness• Also regulates sleep and appetite• 90% of body’s total serotonin located in gut
  • Serotonin• Neurotransmitter associated with feelings of well- being and happiness• Also regulates sleep and appetite• 90% of body’s total serotonin located in gut• Foods with a higher ratio of tryptophan to leucine and phenylalanine increase production of serotonin (bananas, papayas, dates)
  • Serotonin• Neurotransmitter associated with feelings of well- being and happiness• Also regulates sleep and appetite• 90% of body’s total serotonin located in gut• Foods with a higher ratio of tryptophan to leucine and phenylalanine increase production of serotonin (bananas, papayas, dates)• Foods with a lower ratio decrease production of serotonin (wheat, rye bread)
  • Dopamine
  • Dopamine• Dopamine is pleasure and reward neurotransmitter
  • Dopamine• Dopamine is pleasure and reward neurotransmitter• Synthesized from tyrosine via tyrosine hydroxylase
  • Dopamine• Dopamine is pleasure and reward neurotransmitter• Synthesized from tyrosine via tyrosine hydroxylase• Dopamine is precursor for norepinephrine and epinephrine
  • Dopamine• Dopamine is pleasure and reward neurotransmitter• Synthesized from tyrosine via tyrosine hydroxylase• Dopamine is precursor for norepinephrine and epinephrine• Low levels associated with ADHD, Parkinson’s, depression, addictions, and introversion
  • Dopamine• Dopamine is pleasure and reward neurotransmitter• Synthesized from tyrosine via tyrosine hydroxylase• Dopamine is precursor for norepinephrine and epinephrine• Low levels associated with ADHD, Parkinson’s, depression, addictions, and introversion• High levels associated with mania, psychosis, and extroversion
  • Dopamine Synthesis
  • Dopamine Synthesis
  • Dopamine Synthesis
  • L-Tyrosine
  • L-Tyrosine• Synthesized from L-phenylalanine; precursor to dopamine
  • L-Tyrosine• Synthesized from L-phenylalanine; precursor to dopamine• Diet sources include: chicken, turkey, fish, almonds, avocados, cheeses, yogurt, pumpkin seeds
  • L-Tyrosine• Synthesized from L-phenylalanine; precursor to dopamine• Diet sources include: chicken, turkey, fish, almonds, avocados, cheeses, yogurt, pumpkin seeds• A number of studies have found tyrosine to be useful during conditions of stress, cold, sleep deprivation, and improvements in cognitive and physical performance
  • L-Tyrosine• Synthesized from L-phenylalanine; precursor to dopamine• Diet sources include: chicken, turkey, fish, almonds, avocados, cheeses, yogurt, pumpkin seeds• A number of studies have found tyrosine to be useful during conditions of stress, cold, sleep deprivation, and improvements in cognitive and physical performance• Dosing: 1-6 grams/day in divided doses
  • GABA
  • GABA• Major inhibitory neurotransmitter in CNS
  • GABA• Major inhibitory neurotransmitter in CNS• Associated with relaxing, anti-anxiety, anticonvulsant effects
  • GABA• Major inhibitory neurotransmitter in CNS• Associated with relaxing, anti-anxiety, anticonvulsant effects• Synthesized in the brain from glutamate and Vitamin B6
  • GABA• Major inhibitory neurotransmitter in CNS• Associated with relaxing, anti-anxiety, anticonvulsant effects• Synthesized in the brain from glutamate and Vitamin B6• L-theanine, kava, skullcap and valerian are thought to increase GABA peripherally but do NOT cross blood-brain barrier
  • Glutamate
  • Glutamate• Major excitatory neurotransmitter in CNS
  • Glutamate• Major excitatory neurotransmitter in CNS• Involved in learning, memory, and neuroplasticity (long-term-potentiation)
  • Glutamate• Major excitatory neurotransmitter in CNS• Involved in learning, memory, and neuroplasticity (long-term-potentiation)• Excessive glutamate binds to NMDA receptor and causes neuronal death (excitotoxicity)
  • Glutamate• Major excitatory neurotransmitter in CNS• Involved in learning, memory, and neuroplasticity (long-term-potentiation)• Excessive glutamate binds to NMDA receptor and causes neuronal death (excitotoxicity)• Found in cheese, soy sauce, and responsible for umami, one of five basic tastes
  • Glutamate• Major excitatory neurotransmitter in CNS• Involved in learning, memory, and neuroplasticity (long-term-potentiation)• Excessive glutamate binds to NMDA receptor and causes neuronal death (excitotoxicity)• Found in cheese, soy sauce, and responsible for umami, one of five basic tastes• Sodium salt is food additive and flavor enhancer: monosodium glutamate, or MSG
  • Glutamine
  • Glutamine• Conditionally essentially amino acid
  • Glutamine• Conditionally essentially amino acid• Used as source of cellular energy
  • Glutamine• Conditionally essentially amino acid• Used as source of cellular energy• Produced from glutamate; muscle contains 90% of body’s total glutamine stores
  • Glutamine• Conditionally essentially amino acid• Used as source of cellular energy• Produced from glutamate; muscle contains 90% of body’s total glutamine stores• Uses: reduces healing time after operations, decreases muscle breakdown, enhances immunity; increases human growth hormone
  • Glutamine• Conditionally essentially amino acid• Used as source of cellular energy• Produced from glutamate; muscle contains 90% of body’s total glutamine stores• Uses: reduces healing time after operations, decreases muscle breakdown, enhances immunity; increases human growth hormone• Other studies demonstrate stabilizing effect on blood sugar and decreased cravings for alcohol in recovering alcoholics
  • Glutamine• Conditionally essentially amino acid• Used as source of cellular energy• Produced from glutamate; muscle contains 90% of body’s total glutamine stores• Uses: reduces healing time after operations, decreases muscle breakdown, enhances immunity; increases human growth hormone• Other studies demonstrate stabilizing effect on blood sugar and decreased cravings for alcohol in recovering alcoholics• Dietary sources: beef, chicken fish, eggs, wheat cabbage, beets, spinach, parsley
  • Glutamine• Conditionally essentially amino acid• Used as source of cellular energy• Produced from glutamate; muscle contains 90% of body’s total glutamine stores• Uses: reduces healing time after operations, decreases muscle breakdown, enhances immunity; increases human growth hormone• Other studies demonstrate stabilizing effect on blood sugar and decreased cravings for alcohol in recovering alcoholics• Dietary sources: beef, chicken fish, eggs, wheat cabbage, beets, spinach, parsley• Doses: 5-15 grams/day
  • The Yin and the Yang of Neurotransmitters Glutamate is the major excitatory neurotransmitter in the CNS Glutamate GABA GABA is the major inhibitoryneurotransmitter in the CNS
  • Acetylcholine
  • Acetylcholine• Involved with learning and short-term memory
  • Acetylcholine• Involved with learning and short-term memory• Synthesized from B vitamin choline and Vitamin B5, pantothenic acid
  • Acetylcholine• Involved with learning and short-term memory• Synthesized from B vitamin choline and Vitamin B5, pantothenic acid• Dietary sources: eggs and lecithin from soy
  • Acetylcholine• Involved with learning and short-term memory• Synthesized from B vitamin choline and Vitamin B5, pantothenic acid• Dietary sources: eggs and lecithin from soy• Supplements: phosphatidylcholine and phosphatidylserine
  • Acetylcholine• Involved with learning and short-term memory• Synthesized from B vitamin choline and Vitamin B5, pantothenic acid• Dietary sources: eggs and lecithin from soy• Supplements: phosphatidylcholine and phosphatidylserine• Damage to cholinergic neurons associated with Alzheimer’s disease
  • Acetylcholine• Involved with learning and short-term memory• Synthesized from B vitamin choline and Vitamin B5, pantothenic acid• Dietary sources: eggs and lecithin from soy• Supplements: phosphatidylcholine and phosphatidylserine• Damage to cholinergic neurons associated with Alzheimer’s disease• Acetyl-L-carnitine and nicotine stimulate ACh receptors
  • email: mlaramd@yahoo.com Twitter: MichaelLaraMD
  • Endogenous Opiates
  • Endogenous Opiates• Endogenous opiates (endorphins) function as neurotransmitters and are released during exercise, eating, sex, excitement and pain
  • Endogenous Opiates• Endogenous opiates (endorphins) function as neurotransmitters and are released during exercise, eating, sex, excitement and pain• B-endorphin, released by pituitary, is cleavage product from POMC
  • Endogenous Opiates• Endogenous opiates (endorphins) function as neurotransmitters and are released during exercise, eating, sex, excitement and pain• B-endorphin, released by pituitary, is cleavage product from POMC• B-endorphin may have role in mediating runner’s high
  • Endogenous Opiates• Endogenous opiates (endorphins) function as neurotransmitters and are released during exercise, eating, sex, excitement and pain• B-endorphin, released by pituitary, is cleavage product from POMC• B-endorphin may have role in mediating runner’s high• Opiate blockers (naltrexone) used for weight reduction, alcohol abuse and for reducing euphoria associated with self-injurious behaviors
  • Inflammation and Mood
  • Inflammation
  • Inflammation• Response of vascular tissues to harmful stimuli
  • Inflammation• Response of vascular tissues to harmful stimuli• Cytokines are key messenger proteins that regulate inflammatory process
  • Inflammation• Response of vascular tissues to harmful stimuli• Cytokines are key messenger proteins that regulate inflammatory process• Inflammation may have a role in various disease states including depression and Alzheimer’s disease
  • Inflammation• Response of vascular tissues to harmful stimuli• Cytokines are key messenger proteins that regulate inflammatory process• Inflammation may have a role in various disease states including depression and Alzheimer’s disease• Food and eating pattern can be inflammatory
  • Inflammation• Response of vascular tissues to harmful stimuli• Cytokines are key messenger proteins that regulate inflammatory process• Inflammation may have a role in various disease states including depression and Alzheimer’s disease• Food and eating pattern can be inflammatory• Inflammation and stress can lead to accumulation of visceral fat, which in turn can produce inflammatory cytokines and other hormones that affect appetite
  • Inflammation and Cortisol
  • Inflammation and Cortisol• Hypothalamic-pituitary-adrenal axis modulates reactions to stress and regulates mood, energy storage, sex, and immune systems
  • Inflammation and Cortisol• Hypothalamic-pituitary-adrenal axis modulates reactions to stress and regulates mood, energy storage, sex, and immune systems• Cortisol increases blood sugar through gluconeogenesis and suppresses immune system
  • Inflammation and Cortisol• Hypothalamic-pituitary-adrenal axis modulates reactions to stress and regulates mood, energy storage, sex, and immune systems• Cortisol increases blood sugar through gluconeogenesis and suppresses immune system• Altered patterns of in cortisol secretion in many conditions associated with stress, including MDD and PTSD
  • Inflammation and Cortisol• Hypothalamic-pituitary-adrenal axis modulates reactions to stress and regulates mood, energy storage, sex, and immune systems• Cortisol increases blood sugar through gluconeogenesis and suppresses immune system• Altered patterns of in cortisol secretion in many conditions associated with stress, including MDD and PTSD• Leads to accumulation of visceral fat
  • Inflammation and Depression
  • Inflammation and Depression• Increases in stress-induced inflammatory response in depressed patients
  • Inflammation and Depression• Increases in stress-induced inflammatory response in depressed patients• Cytokines induce “sickness behavior” characterized by fatigue and depression
  • Inflammation and Depression• Increases in stress-induced inflammatory response in depressed patients• Cytokines induce “sickness behavior” characterized by fatigue and depression• Exists with other diseases of inflammation: DM II, asthma, CAD
  • Inflammation and Depression• Increases in stress-induced inflammatory response in depressed patients• Cytokines induce “sickness behavior” characterized by fatigue and depression• Exists with other diseases of inflammation: DM II, asthma, CAD• Pro-inflammatory cytokines (IL-1, IL-6, TNF) produce symptoms of depression and anxiety
  • Inflammation and Depression• Increases in stress-induced inflammatory response in depressed patients• Cytokines induce “sickness behavior” characterized by fatigue and depression• Exists with other diseases of inflammation: DM II, asthma, CAD• Pro-inflammatory cytokines (IL-1, IL-6, TNF) produce symptoms of depression and anxiety• Cytokines overactive HPA axis
  • Effects of Cortisol on Hippocampus Andreasen, Brave New Brain: Conquering Mental Illness in the Era of the Genome, 2001
  • Effects of Cortisol on Hippocampus Andreasen, Brave New Brain: Conquering Mental Illness in the Era of the Genome, 2001
  • Effects of Cortisol on Hippocampus Andreasen, Brave New Brain: Conquering Mental Illness in the Era of the Genome, 2001
  • Effects of Cortisol on Hippocampus Andreasen, Brave New Brain: Conquering Mental Illness in the Era of the Genome, 2001
  • Effects of Cortisol on Hippocampus Andreasen, Brave New Brain: Conquering Mental Illness in the Era of the Genome, 2001
  • Telomere Shortening and Mood Disorders
  • Antidepressants and Inflammation
  • Antidepressants and Inflammation• Depression associated with up-regulation of inflammatory response system• Hyperproduction of pro-inflammatory cytokines reversed by antidepressants• Antidepressants decrease gamma interferon and TNF-alpha; and increase anti inflammatory IL-10• Anti-inflammatory drugs currently under investigation as antidepressants
  • Inflammation and Alzheimer’s
  • Inflammation and Alzheimer’s • Most common form of dementia
  • Inflammation and Alzheimer’s • Most common form of dementia • Accumulation of b-amyloid plaques and tau proteins (neurofibrillary tangles)
  • Inflammation and Alzheimer’s • Most common form of dementia • Accumulation of b-amyloid plaques and tau proteins (neurofibrillary tangles) • Evidence of altered immune status in AD
  • Inflammation and Alzheimer’s • Most common form of dementia • Accumulation of b-amyloid plaques and tau proteins (neurofibrillary tangles) • Evidence of altered immune status in AD • Long-term use of NSAIDs may protect against AD but not vascular dementia
  • Projected Changes in Prevalence of AD between 2000-2025
  • Anti-inflammatory Nutrients
  • Anti-inflammatory Nutrients• Anti-inflammatory foods include fruit and vegetables, fish, walnuts, flax and whole grains
  • Anti-inflammatory Nutrients• Anti-inflammatory foods include fruit and vegetables, fish, walnuts, flax and whole grains• Anti-inflammatory spices include sage, ginger, chili peppers, black pepper, and curcumin
  • Anti-inflammatory Nutrients• Anti-inflammatory foods include fruit and vegetables, fish, walnuts, flax and whole grains• Anti-inflammatory spices include sage, ginger, chili peppers, black pepper, and curcumin• Green tea may inhibit atherosclerosis and hypercholesterolemia
  • Anti-inflammatory Nutrients• Anti-inflammatory foods include fruit and vegetables, fish, walnuts, flax and whole grains• Anti-inflammatory spices include sage, ginger, chili peppers, black pepper, and curcumin• Green tea may inhibit atherosclerosis and hypercholesterolemia• Red wine contains resveratol which protects tissues inside blood vessels
  • Anti-inflammatory Nutrients• Anti-inflammatory foods include fruit and vegetables, fish, walnuts, flax and whole grains• Anti-inflammatory spices include sage, ginger, chili peppers, black pepper, and curcumin• Green tea may inhibit atherosclerosis and hypercholesterolemia• Red wine contains resveratol which protects tissues inside blood vessels• Moderate consumption of alcohol raises good cholesterol (HDL)
  • Anti-inflammatory Nutrients• Anti-inflammatory foods include fruit and vegetables, fish, walnuts, flax and whole grains• Anti-inflammatory spices include sage, ginger, chili peppers, black pepper, and curcumin• Green tea may inhibit atherosclerosis and hypercholesterolemia• Red wine contains resveratol which protects tissues inside blood vessels• Moderate consumption of alcohol raises good cholesterol (HDL)• Dark chocolate can reduce blood pressure and elevate mood
  • Anti-Inflammatory Nutrients
  • Alzheimer’s Disease and Mediterranean Diet
  • Omega-3 Fatty Acids
  • Omega-3 Fatty Acids• EFAs are required for normal metabolism but are not synthesized by body
  • Omega-3 Fatty Acids• EFAs are required for normal metabolism but are not synthesized by body• EPA, DHA and ALA
  • Omega-3 Fatty Acids• EFAs are required for normal metabolism but are not synthesized by body• EPA, DHA and ALA• Common sources include breast milk, wild fish, seaweed, algae, and flaxseed
  • Omega-3 Fatty Acids• EFAs are required for normal metabolism but are not synthesized by body• EPA, DHA and ALA• Common sources include breast milk, wild fish, seaweed, algae, and flaxseed• Believed to play key role in maintaining fluidity of cell membranes
  • Omega-3 Fatty Acids• EFAs are required for normal metabolism but are not synthesized by body• EPA, DHA and ALA• Common sources include breast milk, wild fish, seaweed, algae, and flaxseed• Believed to play key role in maintaining fluidity of cell membranes• May also stabilize blood glucose
  • Omega-3s and Depression• Several epidemiological studies suggest covariation between fish consumption and rates of depression• 2004 study found that suicide attempt patients had lower blood levels of Omega-3 fatty acids• Lower blood levels of DHA associated with higher suicide rates among U.S. military• 2007 meta-analysis showed that Omega-3s significantly improved depression in both patients with unipolar and bipolar disorder• Health benefits of Omega-3s may be especially important in patients with psychiatric disorder due to high prevalence of smoking and obesity
  • Antidepressants• SSRIs (fluoxetine, citalopram, sertraline) increase availability of serotonin by blocking reuptake pump• SNRIs (duloxetine, venlafaxine) increase availability of serotonin and norepinephrine• TCAs (amitriptyline, nortriptyline, imipramine, doxepin) increase availability of serotonin, norepinephrine but also activate other receptor subtypes• MAOI (selegiline, tranylcypromine, phenelzine) inhibit enzyme that breaks down serotonin, norepinephrine and dopamine
  • SAMe• Donor of methyl groups in many essential biologic reactions, including the synthesis of neurotransmitters• Efficacy equal to FDA approved antidepressants• Expensive; may induce mania; GI upset; insomnia• Doses range from 200-1,600 mg/day in divided doses
  • Folic Acid• Folate deficiency associated with increased risk of depression• In patients who suffer from depression, 7 out of 10 may have a specific genetic factor that limits their ability to convert folate from diet to L-methylfolate• At risk populations for low folate levels: MTHFR polymorphism, diabetes, hypothyroidism, excessive EtOH and smokers• Drugs that deplete folate include: oral contraceptives, antiepileptic drugs, metformin, methotrexate, niacin• L-methylfolate (medical food product) crosses blood brain barrier to assist in synthesis of neurotransmitters
  • St. John’s Wort• Effective for mild-moderate depression• Response rate 64% v. 59% for TCAs• MOA: the inhibition of cytokines; decrease in 5-HT receptor density• Suggested dose: 900-1,800 in divided doses
  • Stress-Related Eating and Appetite
  • Cortisol and Appetite
  • Cortisol and Appetite• Main hormone associated with chronic stress
  • Cortisol and Appetite• Main hormone associated with chronic stress• Chronic elevated cortisol causes elevated blood glucose, which can lead to type 2 diabetes
  • Cortisol and Appetite• Main hormone associated with chronic stress• Chronic elevated cortisol causes elevated blood glucose, which can lead to type 2 diabetes• Cortisol also increases activity in amygdala, resulting in increased craving for sweet, salty, fatty foods
  • Cortisol and Appetite• Main hormone associated with chronic stress• Chronic elevated cortisol causes elevated blood glucose, which can lead to type 2 diabetes• Cortisol also increases activity in amygdala, resulting in increased craving for sweet, salty, fatty foods• Cortisol increased by loss of sleep, excessive exercise, psychological stress and restrictive dieting
  • Cortisol and Appetite• Main hormone associated with chronic stress• Chronic elevated cortisol causes elevated blood glucose, which can lead to type 2 diabetes• Cortisol also increases activity in amygdala, resulting in increased craving for sweet, salty, fatty foods• Cortisol increased by loss of sleep, excessive exercise, psychological stress and restrictive dieting• Excess cortisol associated with stress of restrained eating and body image disturbance
  • Cortisol and Appetite• Main hormone associated with chronic stress• Chronic elevated cortisol causes elevated blood glucose, which can lead to type 2 diabetes• Cortisol also increases activity in amygdala, resulting in increased craving for sweet, salty, fatty foods• Cortisol increased by loss of sleep, excessive exercise, psychological stress and restrictive dieting• Excess cortisol associated with stress of restrained eating and body image disturbance• Effects of chronic cortisol elevation may be mitigated by omega-3 supplementation
  • Regulation of Appetite
  • Regulation of Appetite• Human appetite control systems designed for survival in primitive times
  • Regulation of Appetite• Human appetite control systems designed for survival in primitive times• Regulated by lower brain structures (amygdala, hypothalamus), dopamine-driven reward circuits, and higher prefrontal cortex circuits
  • Regulation of Appetite• Human appetite control systems designed for survival in primitive times• Regulated by lower brain structures (amygdala, hypothalamus), dopamine-driven reward circuits, and higher prefrontal cortex circuits• Automatic, impulsive eating behaviors associated with primitive brain structures may be overcome by higher prefrontal cortex, responsible for decision-making and planning
  • The Starvation Response
  • The Starvation Response• Biochemical and physiological changes that reduce metabolism in response to lack of food
  • The Starvation Response• Biochemical and physiological changes that reduce metabolism in response to lack of food• During short periods of energy abstinence, body will burn FFA from body fat stores; after prolonged starvation, body will break down lean tissue and muscle
  • The Starvation Response• Biochemical and physiological changes that reduce metabolism in response to lack of food• During short periods of energy abstinence, body will burn FFA from body fat stores; after prolonged starvation, body will break down lean tissue and muscle• Glucose in diet is used first, then stored glycogen, then breakdown of fats into glycerol + free fatty acids
  • Caloric Restriction• Dietary regimen that restricts total calorie intake by 10-25%• CR shown to reduce BP, fasting glucose, fasting insulin (65%), and c-reactive protein• Believed to activate longevity genes (SIRT1) and reduce oxidative stress• Shown to extend lifespan in many organisms, including primates but human studies are ongoing
  • L-tryptophan• Essential amino acid obtained only through diet• Precursor to serotonin and melatonin• Believed to contribute to post-meal drowsiness but mechanism likely involves insulin secretion after high carb meal• Competes with BCAAs and L-tyrosine for passage through blood-brain barrier
  • Dietary Interventions for Psychiatric Conditions• Elimination diets for ADHD have largely failed to identify a single causative nutrient• Medium carbohydrate diet (Zone Diet) for mood disorders• Ketogenic diet for bipolar disorder• Medium-chain triglycerides for Alzheimer’s (Axona)
  • Ketogenic Diets• High-fat, adequate-protein, low calorie diet used to treat epilepsy in children• Evidence for efficacy in Parkinson’s, Alzheimer’s, ALS, traumatic brain injury, stroke• In absence of glucose, liver breaks down fat to free fatty acids and ketone bodies• Ketones cross blood-brain barrier and are used as fuel source• 4:1 ratio of fat: protein+carbohydrates
  • Medium Chain Triglycerides• MCTs are more ketogenic that LCTs, which are more common dietary source of fats• Allows more carbohydrate in diet compared to classic ketogenic diet• Most common source: coconut oil• Used also for weight loss, and by endurance athletes and bodybuilders
  • Blood Sugar, Brain and Behavior
  • Hypoglycemia• Defined as fasting blood glucose < 70 mg/dL• May cause impaired judgement, emotional lability, slurred speech, and ataxia• If blood glucose <55 mg/dL, epinephrine is released from adrenal glands, resulting in shakiness and dysphoria; <10 mg/dL may cause coma• Prolonged hypoglycemia can impair cognitive function and motor control
  • Hyperglycemia• Generally blood glucose > 200 mg/dL• Symptoms include polyuria, blurred vision, arrhythmia, and coma• Prediabetes: Fasting blood glucose 100-125 mg/dL• Skipping meals may increase fasting blood glucose, but insulin response leads to delayed postprandial hypoglycemia
  • Glycemic Index• Glycemic index is the measure of how much and how quickly a food will raise blood glucose, which is then lowered by insulin• Glycemic load is the measure of the total effect of a meal on blood glucose• High glycemic index foods include refined grains products, potatoes, and sugary foods• Low GI foods include legumes, fat-free dairy products, some fruits, and barley• Blood glucose can be stabilized by emphasizing low GI foods, and eating 5 times a day (either small meals, or 3 moderate meals and 2 snacks)
  • Dietary Fiber• Fiber is a diverse group of compounds, including lignin and complex carbohydrates, that cannot be digested by human enzymes in the small intestine• Viscous fibers, such as those found in oat products and legumes, can lower serum LDL cholesterol levels and normalize blood glucose and insulin responses• For adults who are 50 years of age and younger, the AI recommendation for total fiber intake is 38 g/day for men and 25 g/day for women. For adults over 50 years of age, the recommendation is 30 g/day for men and 21 g/day for women
  • Psyllium and Blood Glucose
  • Sugar and The Brain
  • Sugar and The Brain• Brain uses 25% of glucose that is available to body
  • Sugar and The Brain• Brain uses 25% of glucose that is available to body• If blood glucose falls too low, mood can become impatient, irritable, and aggressive
  • Sugar and The Brain• Brain uses 25% of glucose that is available to body• If blood glucose falls too low, mood can become impatient, irritable, and aggressive• Self-control requires adequate glucose in the brain
  • Sugar and The Brain• Brain uses 25% of glucose that is available to body• If blood glucose falls too low, mood can become impatient, irritable, and aggressive• Self-control requires adequate glucose in the brain• Sugar, fat, and salt activate reward circuits in the brain that override prefrontal circuits that govern higher cognitive function such as self-control
  • Insulin Resistance and Prediabetes• Prediabetes is a condition in which blood glucose levels are higher than normal but not high enough for a diagnosis of diabetes• The U.S. Department of Health and Human Services estimates that about one in four U.S. adults aged 20 years or older—or 57 million people—had prediabetes in 2007• Studies have shown that most people with prediabetes develop type 2 diabetes within 10 years, unless they lose 5 to 7 percent of their body weight—about 10 to 15 pounds for someone who weighs 200 pounds—by making changes in their diet and level of physical activity.
  • Obesity Trends* Among U.S. Adults BRFSS, 1990, 2000, 2010 (*BMI ≥30, or about 30 lbs. overweight for 5’4” person) 1990 2000 2010 No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%Source: Behavioral Risk Factor Surveillance System, CDC.
  • Obesity Trends* Among U.S. Adults BRFSS, 1990, 2000, 2010 (*BMI ≥30, or about 30 lbs. overweight for 5’4” person) 1990 2000 2010 No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%Source: Behavioral Risk Factor Surveillance System, CDC.
  • Obesity Trends* Among U.S. Adults BRFSS, 1990, 2000, 2010 (*BMI ≥30, or about 30 lbs. overweight for 5’4” person) 1990 2000 2010 No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%Source: Behavioral Risk Factor Surveillance System, CDC.
  • Appetite Suppressants• Psychostimulants: increase DA and NE• Phentermine: primarily increases NE, but also increases 5-HT and DA• Sibutramine: NE and 5-HT reuptake inhibitor• Bupropion/naltrexone• Orlistat: reduces absorption of fats from GI tract• Natural appetite suppressants
  • Naltrexone• Opioid receptor antagonist used in treatment of alcohol dependence• Believed to reduce dopaminergic activity in reward centers of brain• Used to treat self-injurious behaviors, impulse control disorders (trichotillomania, kleptomania, compulsive gambling)• May reduce reward associated with over-eating and is key component in weight loss drug Contrave
  • Branched Chain Amino Acids• Leucine, isoleucine, and valine are essential amino acids• Used medically to treat ALS, hepatic encephalopathy, and tardive dyskinesia• Used by athletes to improve exercise performance and reduce muscle breakdown during intense exercise• May also blunt the release of insulin and may therefore reduce appetite associated with caloric restriction• Recommended doses: 5-20 grams/day in divided doses
  • Optimizing Sleep and Awareness
  • What is ADHD?• Neurobehavioral disorder beginning in childhood that results in: Inattention • • Impulsivity • Hyperactivity• Causes dysfunction in at least two different areas: • Peer or family relationships • Work or school • Home• Symptoms are not accounted for by another medical or psychiatric condition
  • Nutrients for Improving Attention• SAMe• B-vitamins• Omega-3 Fatty Acids• L-tyrosine• DMAE
  • B-Vitamins and ADHD• B-vitamins are co-factors in the synthesis of monoamines • Most evidence for B-6 (pyridoxine) deficiency, but B-9 (folate) and B-12 deficiencies have been documented• High-stress states deplete body’s stores of B-vitamins• Antidepressants and stimulant medications are known to deplete B-vitamins• Key ingredient in many OTC formulations for ADHD treatment • Focus Factor, Synaptol• Recommend High-Potency, Hypoallergenic B-Complex with meals every morning
  • An Overview of Anxiety Disorders• Generalized Anxiety Disorder• Panic Disorder• Post Traumatic Stress Disorder• Obsessive-Compulsive Disorder
  • Dietary Supplements for Anxiety Disorders• L-theanine• Kava kava• Valerian• Passion flower• GABA• 5-HTP
  • Kava Kava• Controlled, double-blind studies suggest it may be helpful for mild anxiety• Works by conversion to kavapyrones: central muscle relaxants and anticonvulsants• Involved with GABA receptor binding and NE uptake inhibition• Suggested dose: 60-120 mg/day
  • Valerian• Decreases sleep latency and improves sleep quality• Decreases GABA breakdown• Suggested doese is 450-600 mg taken 2 hours before bedtime
  • N-acetylcysteine• Amino acid derivative used as medication and as nutritional supplement• Precursor of antioxidant glutathione• May be useful for OCD, trichotillomania, impulse control disorder, alcohol- and cocaine-related disorders, and schizophrenia• Believed to counteract glutamate hyperactivity via NMDA receptor• For impulse control disorders, dose 600 mg 3-4x/day
  • Magnesium• Functions include relaxation and contraction of muscles and production and transport of cellular energy• Assists with cellular glucose utilization to improve insulin resistance• Deficiency results in hyperexcitability, muscle weakness, and sleepiness• Deficiency common with EtOH abuse, some medications (lasix, HCTZ), malabsorption syndromes• Found in green, leafy vegetables, spinach, and unrefined grains
  • Nutrients for Cognitive Impairment• Omega-3 fatty acids• Ginko biloba• Phosphatidylcholine and phosphatidylserine• B-vitamins• Medium Chain Triglycerides (Axona)
  • Ginko Biloba• Long history of use for treatment of cognitive deficits in AD and vascular dementia• May also improve learning capacity• Year long study with 309 patients suggest that ginko may stabilize and improve cognitive performance in demented patients• Suggested doses: 120-240 mg/day
  • Phosphatidylcholine and Serine• PC is a major component of cell membranes• PC supplementation believed to slow down age-related (oxidative damage) and enhance learning and memory• FDA: “PS may reduce the risk of dementia in the elderly”• PS may reduce exercise-induced stress by blunting response to cortisol
  • Cocoa• Derived from tree theobroma cacao• Rich in flavonoids which protect against coronary heart disease• Health benefits: antioxidant, lowers blood pressure, inhibits platelet aggregation, and reduces inflammation• Intake of flavonoid-rich wine, tea, and chocolate by elderly men and women is associated with better cognitive test performance
  • Chocolate Red Wine Green Tea
  • Sleep and Mood• American adults average 6.5 h sleep, less than most other countries. Optimal functioning reportedly requires 8 ± 0.5 hours• Sleep maintenance through the night may be disturbed by major depression. Generalized and anticipatory anxiety is especially identified with trouble initiating sleep.• Chronic insomnia increases the risk for depression 5 times, the risk for panic disorder 20 times• Patients with major depressive disorder tend to go into REM (dream) sleep shortly after sleep onset,skipping the earlier stages of sleep
  • Melatonin• Hormone derived from serotonin• Effective for people with insomnia caused by circadian rhythm disturbances• Interacts with suprachiasmatic nucleus• Resets circadian pacemaker and attenuates an alerting process• Ambient light inhibits production of endogenous MT• Recommended doses 0.25-3.0 mg/day
  • Summary
  • Summary• Nutrition and Neurotransmitters
  • Summary• Nutrition and Neurotransmitters• Inflammation and Mood
  • Summary• Nutrition and Neurotransmitters• Inflammation and Mood• Stress-Related Eating and Appetite
  • Summary• Nutrition and Neurotransmitters• Inflammation and Mood• Stress-Related Eating and Appetite• Blood Sugar, Brain and Behavior
  • Summary• Nutrition and Neurotransmitters• Inflammation and Mood• Stress-Related Eating and Appetite• Blood Sugar, Brain and Behavior• Optimizing Sleep and Awareness