Craig Lawrence Kien, MD, PhD, received his MD from the University of Cincinnati College of Medicine and his PhD in Nutritional Biochemistry from MIT.  He is a board-certified pediatrician with residency and fellowship training at both McGill and Harvard affiliated hospitals.

Craig Lawrence Kien, MD, PhD, received his MD from the University of Cincinnati College of Medicine and his PhD in Nutritional Biochemistry from MIT. He is a board-certified pediatrician with residency and fellowship training at both McGill and Harvard affiliated hospitals.

Food provides us with nutrients as well as other chemical compounds that can have a positive effect on our health and well-being. For example, the health benefits of polyphenols in olive oil, resveratrol in red wine, and lycopene in tomatoes are well-researched and documented.

There is more to it than just that, though. The biochemistry of what happens when we eat is fascinating.

  • Micronutrients – including vitamins and minerals – and macronutrients – protein, carbohydrate, and fat – provide “energy” to our bodies.
  • Dietary protein repairs and replaces our cells.
  • Carbohydrates provide glucose needed by our brain.

Even fats, by way of their constituent fatty acids, are necessary for normal biochemical function.

  • Palmitic acid, the principal dietary saturated fatty acid (SFA), is necessary for the function of many body proteins and also is a constituent of cell membrane structures, called lipid rafts, which house receptors.
  • Oleic acid, the principal dietary monounsaturated fatty acid (MUFA), “known” for it prominence in olive oil, provides “fluidity” to cell membranes.
  • Linoleic acid and a-linolenic acid, polyunsaturated fatty acids (PUFA) play critical roles in biochemistry.

All of these functions of nutrients are important to keep our bodies running well; however, much controversy, heightened by recent research, surrounds what the ideal “mix” of dietary macronutrients should be in order to minimize the risk of death from coronary heart disease and other disorders related to atherosclerosis (the hardening of the arteries).

It has been known for decades that lowering the blood concentration of “total” cholesterol or “bad cholesterol” (LDL) may be associated with reduced risk for atherosclerosis. However, carbohydrates and various fats differ with respect to how they affect “good” cholesterol, that is, HDL (the former tend to lower it, and the latter raise it).

For many years, it has been known that increasing polyunsaturated fatty acid intake lowers blood cholesterol. Our studies have shown repeatedly that substituting dietary oleic acid for palmitic acid lowers the ratio of blood LDL/HDL, but this does not guarantee a reduced risk of coronary heart disease.

LDL particles, consisting of cholesterol, other fats, and protein, enter blood vessel walls and undergo chemical modification (“oxidation”) and then are engulfed by white blood cells called macrophages. These fat-laden macrophages, called foam cells, create inflammation in the arterial wall, leading to the hardening of the arteries that narrows the lumen of the artery. Palmitic acid activates the chemical pathway leading to such inflammation. Small, very dense particles of LDL penetrate the artery more easily, and saturated fatty acids seem to lower the blood concentration of these particles.

In monkeys, dietary monounsaturated fatty acids are associated with the same risk for atherosclerosis as saturated fatty acids,. Additionally, more monounsaturated fatty acids in LDL increase the probability that the LDL particle will reside longer in the arterial wall and be subjected to chemical modification. Polyunsaturated fatty acids may not be an especially healthy substitute for saturated fatty acids, as suggested by recent re-examinations of large observational studies of how food intake links to death rates and by trials of the effects of saturated fats and polyunsaturated fats on atherosclerosis.

At present, I recommend that those who are at special risk for atherosclerosis should ingest a diet low in saturated fats, with non-protein calories distributed mainly between monounsaturated fats and those dietary starches which tend to resist digestion in the small intestine (high fiber foods such as legumes and whole grains).

Our research, however, is primarily directed at whether high intakes of monounsaturated fats, as opposed to saturated fats, may be associated with lower risk of type 2 diabetes and cognitive decline during aging. Our recent published work suggests that lowering saturated fat intake (from the high levels typical of the Western Diet) may improve risk factors for diabetes and coronary heart disease and improve executive functioning and cognitive control of emotion, resulting in greater physical activity and reduction of negative mood states. Such changes in the brain may reverse negative behaviors but also may impact antecedents of both normal cognitive decline with aging and Alzheimer’s Disease.

Craig Lawrence Kien, MD, PhD, received his MD from the University of Cincinnati College of Medicine and his PhD in Nutritional Biochemistry from MIT.  He is a board-certified pediatrician with residency and fellowship training at both McGill and Harvard affiliated hospitals. Since coming to Vermont in 2004, he has devoted much of his time to research investigating fatty acids, primarily in humans and to teaching nutrition.

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