The document discusses nutrition and chronic diseases. It covers cardiovascular disease, diabetes, and cancer. It describes risk factors for chronic diseases like obesity, physical inactivity, smoking, and diet. It discusses specific diseases like atherosclerosis, hypertension, and metabolic syndrome. It provides recommendations for reducing risk of cardiovascular disease through lifestyle changes, dietary changes, managing diseases, and recognizing symptoms.
Figure 11.1: The Ten Leading Causes of Death in the United States
Many deaths have multiple causes, but diet influences the development of several chronic diseasesānotably, heart disease, some types of cancer, strokes, and diabetes.
Table 11.1: Chronic Disease Risk Factorsa
Of all of these risk factors, the first two are unalterable: you cannot change your age or heredity. As for diseases as risk factors, if you already have one, you may or may not be able to slow or reverse it. The other risk factors have to do with your lifestyle choices and therefore are, to a great extent, under your control. Your choices can be powerful preventive measures against chronic diseases.
Figure 11.2: Interrelationships among Chronic Diseases
Many chronic diseases are themselves risk factors for other chronic diseases, and all of them are linked to obesity. The risk factors highlighted in blue define the metabolic syndrome (defined on p. 412).
Figure 11.3: The Formation of Plaques in Atherosclerosis
Most people have well-developed plaques by the time they reach age 30.
Figure 11.4: A blood clot
A blood clot in an artery, such as this fatal heart embolism, blocks the blood flow to tissues fed by that artery.
Figure 11.6: Know Your Blood Pressure
The most effective single step you can take against hypertension is to learn your own blood pressure.
Figure 11.5: Adult Standards for Blood Lipids
Figure 11.8: The American Heart Associationās Heart Attack Risk Calculator
This online calculator can assess your risk of having a heart attack. For a meaningful assessment, youāll need some information about your blood lipids, blood pressure, and fasting blood glucose. To access the calculator, visit the American Heart Association website: https://professional.heart.org/professional/GuidelinesStatements/ASCVDRiskCalculator/UCM_457698_ASCVD-Risk-Calculator.jsp
When diets are rich in whole grains, vegetables, and fruit, life expectancies are long.
Table 11.5: How Much Does Changing the Eating Pattern Lower L D L Cholesterol?
For those who need to lower low-density lipoprotein (L D L) cholesterol, this table offers a perspective on the magnitude of results that may be possible.
Figure 11.10: Risk-Benefit Relationships
Figure 11.11: Cancer Development
Many consumers appreciate the availability of bacon without added nitrites or nitrates.
Figure 11.12: Examples of Cruciferous Vegetables
Cruciferous vegetables belong to the cabbage family: arugula, bok choy, broccoli, broccoli sprouts, brussels sprouts, cabbages (all sorts), cauliflower, greens (collard, mustard, turnip), kale, kohlrabi, rutabaga, and turnip root.
Regular intake of whole foods like these, not individual chemicals, lowers peopleās cancer risks.
Table 11.9: Recommendations and Strategies for Reducing Cancer Risk
Figure 11.13: Proper Nutrition Shields against Diseases
A well-chosen diet can protect your health.
Figure C11.1: Nutritional Genomics
Two branches of nutritional genomics may have similar-sounding namesānutrigenomics and nutrigeneticsābut they oppose each other in scope. One branch studies how genes affect nutrient metabolism. The other branch studies how nutrients affect the genes.
Figure C11.2: Two Epigenetic Factors and Gene Activity
This figure depicts histones, large globular protein āspoolsā that wrap lengths of D N A. Other epigenetic factors also exist, such as the methyl groups in this illustration, tiny one-carbon structures that attach directly to a D N A strand, modifying its activity. Another is a form of R N A (not shown).
Figure C11.3: An Epigenome Timeline
Environmental influences, including diet, most profoundly alter the epigenome during the earliest stages of development, but some changes are probably still possible later in life.
These two mice share an identical gene that tends to produce fat, yellow mice. The mother of the lean, brown mouse received supplemental B vitamins that silenced the gene.