Cholesterol

Trans fatty acids are produced when an unsaturated fatty acid is exposed to high temperatures (which is why to preserve the natural cis configuration, cold-pressing of the vegetable oils are recommended). The slight difference in the structure between a trans and cis bond has a dramatic effect on the shape and function of the fatty acid. In nature, whether in animals or in plants, the carbons on either side of the double bond are in the cis conformation that results in a bend in the fatty acid chain. On the other hand, the trans conformation results is a straighter and more elongated fatty acid chain that can align closer together with other fatty acids, and therefore is more solid and more sticky, which encourages deposition into arteries, organs, and platelets. (Saturated fats are even stickier). For the same reasons, trans fatty acids also get in the way of cis fatty acid interactions with enzymes and with the function and permeability of cell membranes (saturated fatty acids do not). Trans fatty acids are useful only to the body as energy-creating fuel and are broken down at a slower rate than cis fatty acids. Since trans fatty acids are more stable than cis double bonds, the chance of being converted into the more desirable cis configuration is unlikely. The main dietary source of trans fatty acids is from partial hydrogenation. Read a few labels from cereals, crackers, chips, snacks, instant hot chocolate, salad dressing, etc. to see just how much partially hydrogenated oil the average American consumes without suspecting it. There are no known natural trans fatty acids. From the same study that showed nuts reduce cardiovascular deaths to 82%, the regular consumption of donuts not only increased the mortality from coronary heart disease 210% but also death from any cause 140% compared to those that did not consume donuts regularly (Arch Intern Med 1997;157:2249-58).

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From JAMA (Dec 24, 1997), 832 men were followed for up to 20 years. Those with a low fat and/or a low saturated fat intake had a much higher incidence of stroke events. With higher and lower polyunsaturated fat intake the effect was not as significant. The lesson here is that low fat is detrimental which is not to say that high fat diets are necessarily beneficial.

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Trans fatty acids can increase cholesterol and triglyceride levels. In a study done at Harvard on 85,000 nurses, there was a 50% greater incidence of heart disease among those women consuming the most trans fatty acids compared to those consuming the least. The researchers concluded that “consumption of partially hydrogenated vegetable oil may contribute to the occurrence of heart disease.” (Willett Lancet 1993) Recently the medical literature has been more vocal about their concern over margarines, trans-fatty acids, partial hydrogenation, etc.

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Another critical component of lipid metabolism warranting discussion is that of eicosanoids popularized by Barry Sears, Ph.D. in his book, The Zone. Emmanuel Revici, M.D. provided the early conceptual model for this entire field of fat metabolism. Eicosanoids are a group of powerful chemical mediators that are derived from essential fatty acids and control virtually every aspect of metabolism and physiology. Prostaglandins, leukotrienes, and thromboxanes are among the better described eicosanoids. As in most biological systems, there is a balance among opposing eicosanoids — the series 1 pathway components (generally associated with beneficial activities) and the series 2 pathway components (generally associated with less desirable activities such as inflammation). The biochemistry of those factors that favor the series 1 eicosanoids over the series 2 eicosanoids have focused on the role of a critical enzyme that directs fats down the series 2 pathway — the delta 5 desaturase enzyme. The enzyme is activated by insulin and therefore excessive carbohydrates or carbohydrates with a high glycemic index, aging, stress, viral infection, saturated fats, alcohol, and deficiencies of vitamins and minerals. Strategies for controlling eicosanoids into a favorable balance, called “The Zone,” is the subject of Dr. Sears book and another excellent text, Protein Power, by Michael Eades, M.D.

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Any discussion of fats cannot be complete without including carbohydrates, since sugars and starches can be converted into fats. Refined carbohydrates such as table sugar, fructose, syrups, puffed cereal grains, processed flours, and honey provide an excellent source of energy, but if there is no activity or exercise requiring this energy, then the body has an excess supply of glucose. The capacity to rapidly raise blood sugar is called the glycemic index. Normally, the body responds to high levels of glucose by stimulating the pancreas to secrete insulin, which stimulates the metabolism of glucose into fats for storage in fat tissue or in various organs. The fatty acids produced from glucose metabolism are saturated and therefore can only serve as fuel. In addition, high blood sugar inhibits the release of the essential fatty acid, linoleic acid, from storage fat. This could exacerbate essential fatty acid (EFA) deficiency despite having adequate stores of EFA. Complex unprocessed starches, in contrast to refined sugars, are not as rapidly absorbed and do not cause as dramatic a rise in glucose, the excess glucose. The glucose is absorbed slowly and thus provides a relatively lower, and more prolonged level of blood glucose energy; hence, a lower glycemic index.  It is no surprise that a Denmark study showed that “fasting serum insulin level is a very good predictor of the development of CHD and CVD…”

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According to an article in the Journal of Cardiovascular Risk, June 1995, “All dietary carbohydrates increase insulin levels. Excess carbohydrates cause elevated insulin levels…”

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Angina can be induced by hypoglycemia (Am Heart J 1943;26(2):147-163)

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Insulin promotes delta-5 desaturase activity lead to increased pro-inflammatory eicosanoid production. Impaired sugar metabolism stimulates adrenal exhaustion through blood sugar feedback attempts to increase blood sugar lead to excess potassium, menopause & andropause, etc.

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Vegetables in general lower insulin. Mung beans and other legumes (soybeans), Bitter gourd (Momordica charantia), Ivy gourd (Coccinia indica), Brassica (cabbage, broccoli, cauliflower), green leafy vegetables, omega-3 fatty acids (fish oils), anti-oxidants (vitamin E), alpha-lipoic acid, possibly L-arginine (via NO pathway), chromium/glucose tolerance factors, vanadium, and inositols (d-chiro inositol is important in the construction of membrane proteoglycans that maintain insulin sensitivity).

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Syndrome X is defined as “insulin resistance + hyperinsulinemia” usually accompanied by elevated lipids, body weight, and blood pressure.  The result is reduced cellular glucose transport. Insulin affects gene expression by altering transcription factors that affect triglyceride and cholesterol synthesis and degradation, inflammatory cytokine release, shunting of estrogen to testosterone in women (PCO). Hyperinsulinism contributes to atherosclerosis, hypertension, hyperlipidemia, obesity, and diabetes.

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Low blood sugar levels lead to thyroid, anterior pituitary, adrenal cortex, and sex hormones release. High blood sugar levels lead to insulin, posterior pituitary, and sex hormone release.

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As a result of the Page Food Plan (dominated by protein and vegetables), which is found under my web pages for food programs, the avoidance of sugar based on the reasons above, one will quickly realize that the intake of protein necessarily goes up. This has raised concerns about over-consumption of protein and its effect on osteoporosis, etc. The British Medical Journal (October 1997) included a study of 3600 Britons over a seven-year period. The results show no correlation between meat consumption and cancer. Fresh fruits and vegetables intake as expected had a protective effect. The other concern with increased protein intake has been with promoting osteoporosis due to the systemic acidification that results from protein metabolism. The fact is that the Framingham Osteoporosis Study carried out over a four year period found that individuals with the lowest protein intake had increased rates of bone loss compared to those with higher intakes. In this study, the women who had the highest percentage protein intake had no bone loss at all during the study period. Another study in Switzerland showed the same findings – higher protein intake was associated with greater bone density. A Chinese study of elderly females found lower bone mineral densities in vegetarians than in omnivores. There was no difference between the lactovegetarians and the vegetarians with regard to bone mineral density. Concern over consistent protein intake as recommended by Page contradicts these observations.

 

OTHER FACTORS INVOLVED IN CHOLESTEROL AND LIPID METABOLISM

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Steroid hormones play an important role in cholesterol metabolism. After all, cholesterol is a precursor to steroid hormones, including progesterone, cortisol, estrogen, and testosterone. In Denmark, testosterone has been used as a cholesterol-lowering agent for decades. They report the average reduction in serum cholesterol after testosterone initiation in males is about 25%. A 1972 World Health Organization (WHO) symposium also provided evidence that testosterone had cholesterol-lowering effects as well as increased clot dissolution, and reduced the adhesiveness of platelets (by reducing the amount of the pro-aggregation effect of ADP). Testosterone also induced suppression of lipoprotein (a) levels (Marcovina SM in Atherosclerosis 1996; 122: 89-95). These are all traditional parameters of heart disease risk. Confirming the association between testosterone and heart disease, Gerald Phillips, M.D. at ColumbiaUniversity Medical School, showed that men with the lower levels of testosterone had greater x-ray evidence of coronary artery blockage. Maurice A. Lesser, M.D. injected testosterone to 100 patients during an angina attack with “moderate to marked” improvement in 91%.

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Testosterone shifts metabolism from an anaerobic state to an aerobic one by increasing the activity of enzymes in the Krebs cycle, which increases the level of ATP relative to ADP, which affords the changes mentioned above as well as a variety of other metabolic effects. Testosterone also balances glucose homeostasis by antagonizing glucocorticoids and insulin. It has also been shown “to have a direct effect on reducing blood sugar,” in addition to lowering the insulin requirements of diabetics and improving insulin resistance (J New Drugs 1965; 5: 108-224). Testosterone therapy has been useful for a variety of degenerative conditions. Clearly, the notion that testosterone is merely a sex hormone is to discount the profound effects it has on metabolism – rather it should be considered an anabolic steroid in both males and females. Testosterone also stimulates protein synthesis and decreases protein breakdown leading to improved nitrogen balance. Some common clinical findings with testosterone insufficiency are fatigue, reduced muscle energy, decreased secondary sex characteristics, reduced temperature, reduced blood pressure, cold sweaty hands, frequent/excessive urination, anemia, and compensatory prostatic hypertrophy. The blood chemistry may show low phosphorus.

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Another factor involved in the balancing role of testosterone is its relationship to saturated fat intake. In a study done inFinland, a diet containing only 25% saturated fat decreased testosterone levels by 15%. The same effect occurred when the ratio of polyunsaturated fats was increased compared to saturated fats.

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“Observational studies have consistently shown that estrogen replacement therapy (ERT) is associated with lower overall mortality rates. The effects on deaths due to coronary artery disease (CHD) are striking: a pooled relative risk (RR) of 63%…” (Arch Intern Med 1997;157: 2181-7). However, women who use estrogen were more likely to have healthy habits and characteristics such as not smoking, less overweight, etc. Again, the cause and effect remains uncertain. According to Joseph Collin’s 1999 book on endocrine function, estrogen has powerful anti-oxidant effects.

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Estrogen has several other effects related to cardiovascular efficiency including lowering LDL levels, increasing HDL levels, decreasing Lp(a) levels, affecting endothelin-1, decreasing homocysteine levels and enhancing the effects of B-6, B-12, and folic acid supplementation, decreasing the risk of hyperinsulinemia, and possibly lowering fibrinogen levels and platelet aggregation.

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Conventional care for those women with a uterus and who take estrogen in any form, progesterone are considered mandatory to offset estrogen’s uterine cancer-promoting effects. The most commonly used form of progesterone is the synthetic derivative, methoxyprogesterone (MPA for short), Provera®. Unfortunately, a study published in March 1997 Nature Medicine showed that “moderate levels of MPA interfere with the protective effects of estradiol (E [2]) against coronary reactivity and vasospasm…” This is not to say that progesterone itself is detrimental. This distinction between natural progesterone and synthetic progestins like Provera can not be overemphasized.

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Excess cortisol, on the other hand, not only raises blood lipids and cholesterol, but also promotes the breakdown of protein. Tissue damage, high blood sugar, sympathetic overflow, psychosocial stress leads to ACTH secretion from the anterior pituitary and subsequent cortisol release from the adrenal cortex. Testosterone counteracts this effect and normalizes carbohydrate metabolism with reported marked improvement in pathological glucose tolerance. Confirmation of this effect was recently published by IR Reid in Osteoporosis International (1996;6(suppl 1):274) in 15 asthmatic men receiving long-term oral steroid therapy. Bone density and muscle mass increased while body fat declined. Testosterone also improves circulation with many reports of healing of gangrene, etc. Since cardiac output is the ultimate determination of workload capability of the heart (i.e. the primary marker of health), it is worth understanding how the adult improves cardiac output when the demand arises. We know cardiac output = stroke volume ´ heart rate. It is a fact that, after the age of thirty, the maximal cardiac output declines. The primary way the body stimulates greater output is to increase the heart rate through an increase in the production of catecholamines. Testosterone tempers the metabolic effect of increased catecholamines as well. Goodman and Gillman’s The Pharmacologic Basis of Therapeutics (1980) reported “large or repeated doses of catecholamines given to experimental animals lead to damage to arterial wall and myocardium so severe as to cause the appearance of necrotic areas indistinguishable in the heart from myocardial infarcts.” This tells us that atherosclerosis (and cholesterol) alone must be appreciated for a rational approach to prevention and management of heart disease. A high level of stress with greater overall production of catecholamines and cortisol then must be offset by the balancing effect of other hormones, of which testosterone is included. One could put this in context of Revici’s dualism — the battle and balance between insufficient oxidation and excessive oxidation. For our patients with cortisol excess, either due to stress or medication, should we provide testosterone? Perhaps this is why tranquilizing products such as Min-Chex (Standard Process) that combine the minerals known to balance to autonomics (catecholamines) with a source for testosterone production to balance the hormones (cortisol) are so effective.

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Another adrenal hormone is DHEA, which can be useful addition in select individuals. I would not recommend using it, however, without appropriate medical guidance.

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At the meeting of the American College for the Advancement of Medicine in October 1997, a speaker reported that a persistently low HDL suggested pituitary hypo-function. Other lab findings include an increase in total cholesterol, low thyroid function tests, and a high fibrinogen. At the 1996 American Academy of Anti-Aging Medicine seminar in Las Vegas, Dr. Bengt-Ake reported that deficiency of growth hormone is apparently associated with an increase in atherosclerosis and cardiovascular mortality. Growth hormone has been considered an insulin antagonist. Adult growth hormone deficiency may be characterized by sagging cheeks, deep and large wrinkles, thin hair, lips, jaw bones, and skin, pseudogynecomastia, an obese floppy belly, general muscle loss, fatigue, somnolence, lack of self-assurance and esteem, anxiety, and low sociability. A mixture of arginine, lysine, ornithine, and glutamine can be used to induce growth hormone release. A variety of nutritional products have been developed claiming to stimulate the pituitary to release growth hormone. Other stimulators of growth hormone include hypoglycemia, exercise, sleep, estrogen,glucagon, and stress. Growth hormone itself, albeit in minute amounts, can be purchased over-the-counter while recombinant growth hormone is available through physicians as an injectable.

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Insulin-like Growth Factor-1 (IGF-1) is a derived from metabolism of Growth Hormone in the liver. Effective Growth Hormone therapy elevates IGF-1 and IGF-1 itself has been shown to decrease insulin levels, increase stroke volume, reduce vascular resistance, and lower the filling pressures of the right and left heart.

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In continuing our discussion of hormones, thyroid hormones play a major role in cholesterol metabolism and in atherosclerosis. Advocates of thyroid hormone use report over 50 percent of Americans have low thyroid function, and thyroid hormone levels within the normal range do not exclude a functional deficiency/insufficiency. Gubner and Lange showed hypothyroidism was associated with increased permeability of arteries and less strength of capillaries. A significant percentage of individuals with hypothyroidism have elevated cholesterol. In a study of 279 women, 12% with cholesterol >240mg% had an elevated TSH (Amer J Med; June 1998).

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From Melvin Page, DDS and other endocrinologists, it is known that blood calcium, phosphorus, and cholesterol levels are controlled by the thyroid. With low thyroid function, a relatively high calcium, low phosphorus and high cholesterol is found. With elevated thyroid function, a relatively low calcium, high phosphorus and low cholesterol is found. Of course there are other influences on these levels beside thyroid, but with thyroid replacement, one should be able to predict the resultant changes in calcium, phosphorus, and cholesterol. The balance between calcium and phosphorus is among the most important markers of biochemical homeostasis ever identified. For further discussion, see later text.

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Because there is much confusion about thyroid hormone replacement or glandular support, a brief review of thyroid metabolism is warranted. The thyroid gland secretes thyroxine (T[4]) and a small amount of tri-iodothyronine (T[3]). About 30% of T[4] is de-iodinated to T[3] and 40% de-iodinated to reverse-T[3] (rT[3]) in the periphery. Both T[4] and T[3] are metabolized in the liver by glucuronidation and sulfation. References state that T[3] is about three times* as active as T[4] on target tissues and is the principal regulator of thyroid action within the pituitary; rT[3] has no activity. (*There are some reports that T[3] has nine times the activity of T[4]). Dopamine and glucocorticoids reduce the pituitary’s stimulus to secrete Thyroid Stimulating Hormone (TSH). It has been reported that an excess of polyunsaturated oils, cabbage, soy foods, and improperly prepared nuts and lentils, and beta-carotene suppress thyroid function. Consider liver dysfunction or providing bioactive sulfur if thyroid support is being taken and there is no clinical response. Thyroid function can be adjusted with more than just hormones. To stimulate the thyroid, give phosphorus, polyunsaturated FA (pulls iodine out of the gland), or provide sympathetic ANS support. To depress the thyroid, give calcium, iodine (pharmacologic dose), or provide parasympathetic ANS support. It is worth noting that there is often confusion about the use of iodine with thyroid dysfunction. When there is insufficient iodine, supplemental iodine provides support for the gland. When given in excess, iodine suppresses the thyroid. One last caveat that many practitioners have observed – whenever appropriate therapy of any kind or for any reason does not provide a clinical response, consider thyroid support.

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The recent popularity of soy products has raised some concerns. Not only with regard to its phytoestrogen content, but because it will be marketed in high potency and in a processed form… This is not the forum for a more thorough review but I’m going on records as having a great concern about the intake of high amount of soy. The average daily consumption of soy protein in the Orient is only a few milligrams.

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Many clinical trials have shown phosphatidylcholine reduces total cholesterol and triglycerides by as much as 20-30% as well as a marked improvement in the pathological lipoprotein patterns. Overall, the profile that has been associated with the development of atherosclerosis improves including increases in HDL cholesterol. Phosphatidylcholine also increases the mobilization of cholesterol from pre-existing atheromas to the liver for metabolism and ultimate excretion as bile acids. Improvements in atherosclerotic vascular changes have been shown by several objective measures as well as in reducing symptoms of angina pectoris, cerebral circulatory disorders, and peripheral vascular disease. It is interesting to note that a study showed choline conserved carnitine (J Clin Nutr 1996;63:904-10). It is nice to get the confirmation that the balanced, comprehensive approach we’ve watched in clinical practice work more successfully than a piecemeal fractionated approach is supported in research. Lecithin is an excellent whole food complex rich in phosphatidylcholine. Symptoms suggestive of a need for lecithin include stiffness and bone spurs (phosphorus deficit), vasomotor disturbances (nerve sheath integrity), gallbladder symptoms, and an intolerance to ingested fats (complements bile in emulsification), lipomas and elevated cholesterol (lipid transporter), and forgetfulness (memory occurs in the acetylcholine-rich hippocampus).

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Niacin has long been used for cardiovascular conditions, especially involving lipid metabolism. The use of niacin for managing lipid markers for cardiovascular disease is well established:

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• Reducing LDL and Total Cholesterol (5-25%)

• Increasing HDL Cholesterol (15-35%)

• Decreasing Triglycerides (20-50%)

• Increase in Apolipoprotein A1

• Decrease in Apolipoprotein B

• Shift to larger (less atherogenic) LDL particles

• Reduction in Lipoprotein (a)

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It also may help Raynaud’s Disease (excessive blood vessel constriction due to cold and symptoms of intermittentclaudication) due to insufficient blood supply to calf muscles while walking. Niacin lowers VLDL formation in the liver by activating phosphodiesterase and inhibiting adenylate cyclase which results in the reduction of cyclic AMP in fat cells which in turn reduces the release of free fatty acids from fat cells. As a result, serum VLDL, LDL, triglycerides, phospholipids, and cholesterol are decreased. Niacin also inhibits the formation of cholesterol from acetate in the liver and appears to increase its breakdown as well. There is also evidence lipoprotein A2 synthesis is reduced by niacin and that niacin converts the smaller easily oxidized LDL into larger, oxidation-resistant LDL particles.

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Niacin is part of the alcohol insoluble and heat labile fraction of vitamin B (named the “G” complex that includes riboflavin, niacin, folic acid, PABA, choline, inositol, and betaine). As part of the “G” complex, it relaxes nerves and thereby acts as a vasodilator, helping selected individuals with hypertension and smooth muscle spasm without tone. According to Compiled Notes on Clinical Nutritional Products by Wally H. Schmitt Jr., D.C. (1990) and Vitamin News (1952), signs of “G” deficiency include:

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According to Robert Peshek, DDS the “G” fraction of B-complex allows chloride to enter the cell, just as Valium does. Also raises cholinesterase levels. In fact checking the level of rbc-cholinesterase levels can be a guide to functional need for “G.”

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1. Cardiovascular – tachycardia, extra ventricular beats (PVC’s), angina pectoris, and pre-myocardial infarction

2. Psychological – excessive worry, apprehension, moodiness, depression, suspicion

3. Digestive – insufficient stomach acid production and excess alkalinity, spastic gall bladder

4. Liver – cirrhosis and loss of fat metabolism activity, deficient formation of Yakitron, a physiologic anti-histamine

5. Neurological – insufficient acetylcholine activity and cholinesterase activity (for breaking down acetylcholine and for recycling choline), restless, jumpy, or shaky legs, body or limb jerks upon falling asleep, can hear heartbeat on pillow

6. Skin and mucous membranes – cheilosis (cracking at corners of mouth), friable skin, especially on face and neck (when shaving), bright red tongue tip, strawberry tongue (purple), loss of upper lip (thin upper lip), irritated mucous membranes of the rectum, vagina, and conjunctiva (frequent crying), excessive oil on face and nose, roughness, cracking and exfoliation of the soles of the feet, and psoriasis

7. Visual – burning or itching of eyes, photophobia (sun sensitivity), blepharospasm (eyelid spasms), blood shot eyes due to capillary engorgement, seeing only parts of printed words (circumcorneal injection), pallor of the temporal half of optic disc, transient ischemia of retina – like looking through a fish bowl

8. Endocrine – excess estrogen and menstruation, cystic mastitis or gynecomastia, premenstrual tension, and excessive adrenal function.

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Note: You may be wondering what the evidence for oral exam findings has to do with the heart. The Medical Tribune ran an article in May 1999 correlating the degree of gum disease with the degree of carotid artery plaque… I’m not making this up.

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Niacin is also part of glucose tolerance factor (GTF) which is necessary for proper glucose homeostasis, in part by acting in concert with insulin to improve the body’s responsiveness to insulin. As a result, less insulin is required to accomplish blood glucose regulation. Insulin reduces DHEA and increases the production of the pro-inflammatory eicosanoids such as arachidonic acid. Interestingly, the other part of the vitamin B complex that is alcohol soluble, named the “B” fraction, is combined with even a larger amount of niacin than the commercially available “G” complex per tablet, and yet it has an opposite effect in terms of nerve transmission, heart function, blood vessel tone, and other metabolic functions. Wheat germ has been shown to bind irreversibly to the insulin receptor and mimic its function, thereby creating an artificial insulin effect. It is not known whether sprouting and/or de-fatting the wheat germ changes this effect.

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Niacin is often sold as a timed-released or sustained release product to reduce the flushing that is common when using the high dosage required to effect laboratory benefit.  Niacin is metabolized by two pathways.  One pathway is through conjugated with Glycine resulting in Nicotinuric Acid (NUA).  This results in most of the benefits of niacin mentioned above but also produces the flushing.  Niacin can also be converted to niacinamide (NAM) and other metabolites which are harmless at lower levels but can be potentially hepatotoxic at doses exceeding 1.5 grams per day.  The goal of a sustained-release niacin product is to release as much niacin via the first pathway (NUA) without causing flushing, while fully releasing all the niacin before the secondary pathway is able to form potentially hepatotoxic metabolites. This may be alleviated by using a wax-matrix tablet to achieve a release profile of 45% release within the first hour, 55% release by two hours, 85% in the 3.5 hour, and 90% in 7 hours (www.orthomolecularproducts.com)

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Pantethine has been shown in several studies to lower cholesterol as well as inhibit the oxidation of LDL. In the cytoplasm of the cell, pantethine promotes lipid formation at the expense of cholesterol. In the mitochondria, pantethineaccelerates the beta-oxidation of fatty acids and enhances the metabolic flow into the energy-producing Krebs cycle. During conditions of inadequate blood supply, pantethine improves cellular energetics. Pantethine is a derivative ofpantothenic acid (vitamin B5).

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When all is said and done, ideal cholesterol levels for adults is probably 180-200mg% with concern when it drops below 160mg% or when it is higher than 240mg%. For HDL (the “good” cholesterol), a level of >60 is worth shooting for. A LDL (the “bad” cholesterol) should be less than 140mg%. Triglycerides should be <100mg%.  Apolipoprotein A1 / B ratio should be < 0.7 with an apolipoprotein B level <84.