Nutritional Factors in the Prevention & Treatment of Cardiovascular Disease

In October of last year, Alan Gaby, MD was interviewed in a teleconference on the topic of Nutritional Factors in the Prevention and Treatment of Cardiovascular Disease. I thought you’d be interested in reading my notes… an almost complete-verbatim transcript of his presentation. Very useful and relevant tips beneficial for everyone.

Enjoy.

Jackie

Meet Alan Gaby, M.D.
Dr. Gaby received his undergraduate degree from Yale University, his M.S. in biochemistry from Emory University, and his M.D. from the University of Maryland. He was in private practice for 17 years, specializing in nutritional medicine. He is past-president of the American Holistic Medical Association and gave expert testimony to the White House Commission on Complementary and Alternative Medicine on the cost-effectiveness of nutritional supplements. He is the author of Preventing and Reversing Osteoporosis (Prima, 1994), and The Doctor’s Guide to Vitamin B6 (Rodale Press, 1984), the co-author of The Patient’s Book of Natural Healing (Prima, 1999), and has written numerous scientific papers in the field of nutritional medicine. He has been the contributing medical editor for the Townsend Letter for Doctors since 1985, and contributing editor for Alternative Medicine Review since 1996. He was professor of nutrition and a member of the clinical faculty at Bastyr University in Kenmore, WA, from 1995 to 2002. He is Chief Science Editor for Aisle 7 (formerly Healthnotes, Inc). He has recently completed a 30-year project, a textbook of nutritional medicine. (see references)

VITAMIN E
Alpha tocopherol… around 1950 a colleague of the Shute Bros found injections useful for heart failure patents, so over the years, vitamin E got a reputation for treating heart failure and other types of heart disease. Then in 2005 there was a followup study from the HOPE (Heart outcomes prevention evaluation) very large clinical trial where they gave 400IU vitamin E a day and followed them for 6 – 7 years and there was a 19% increase in the incidence of heart failure in previously non-cardiac patients in those who took vitamin E compared with those who took placebo. So that got a lot of press and it was published around the time of another study – a meta-analysis showed that 400 IUs a day of vitamin E or more had a slight but statistically significant increase in mortality of about 4% compared with placebo so vitamin E fell out of favor around that time and most cardiologist recommending it stopped doing so.

The problem is that vitamin E and alpha tocopherol are not synonymous. Vitamin E as it occurs in food contains alpha, beta, delta and gamma tocopherol. Since the 1920’s when vitamin E was discovered, we assumed that alpha was the only active substance since it prevents vitamin E deficiency as determined in rat studies by fetal resorption assay results and none of the other forms of vitamin E can do that.

However, in the last 15 years, we discovered numerous positive effects of Gamma Tocopherol. For example, it’s antioxidant function, it is a more potent platelet aggregation inhibitor than alpha tocopherol and perhaps the greatest import it functions as a natriuretic hormone natri meaning to excrete sodium. This was identified at Loma Linda University. So there is a breakdown product of Gamma Tocopherol known as Gamma CEHC which does that and one can postulate that if your natriuresis is messed up, then every time you consume salt and fluid it will put additional stress on your heart and; therefore, adequate Gamma tocopherol may be necessary to preserve cardiac function over the years.

It has also been demonstrated very clearly now that high dose Alpha tocopherol causes a depletion of Gamma tocopherol – sometimes in as little as 48 hours.

So the bottom line, and this is still speculative, but there is strong circumstantial evidence to support that Alpha tocopherol, by itself, despite certain benefits on the cardiovascular (CV) system such as antioxidant function, such as inhibiting platelet aggregation, is counterbalanced by alpha tocopherol-induced gamma-tocopherol deficiency and if one uses mixed tocopherols, one would not expect those adverse effects to occur and might expect the beneficial effects as reported back in the 1950’s.

There is still research that needs to be done. I and others agree we need to go back and redo all of the alpha tocopherol research but that work has not dissuaded me from recommending mixed tocopherols to my patients.

DIET AND PREVENTION OF ATHEROSCLEROSIS…
The standard belief system (not necessarily wisdom) from way back in the 60’s was that dietary cholesterol and saturated fat was bad and polyunsaturated fats were good… they didn’t say. much about sugar except John Yudkin over in England has been yelling about sugar for about 40 or 50 years… it turns out that it is much more complicated than that and some of it is actually wrong. I can tell you my take on it and we’ll get to that in a few minutes.

A recent meta-analysis of 21 studies published in the American Journal of Clinical Nutrition showed no correlation of intake of dietary fat and incidence of cardiovascular disease. So…that one is kinda kicked by the wayside. Saturated fat is metabolized in the body and while it may raise triglyciderides to some extent, it doesn’t seem to do much else that would predict cardiovascular risk.

In addition, as you all know, cholesterol is an essential nutrient and if one does not ingest it, the liver will synthesize it because we need it as a precursor to steroid hormones and we need it as a component of cell membranes.

So why would high cholesterol saturated high saturated fats be bad for us? They may be-- but for reasons perhaps unrelated to their saturated fat content. For one, most of the foods high in cholesterol and saturated fats are meats. And when we cook them (and we have to cook them to avoid some kind of infectious disease) particularly at high temperatures, a number of toxic by-products are formed – one is oxidized cholesterol which is highly atherogenic even though even though pure native cholesterol does not produce atherosclerosis in animals. If it is allowed to oxidize, then it produces atherosclerosis even at low doses. The same thing may occur with the various unsaturated fats when heated to high temperatures, those oxidize and form lipid peroxides. Third, when you heat meats and other foods to high temperatures, it causes the formation of Advanced Glycation End-products – AGEs… nice acronym because they do accelerate the aging process as well.

So, heavily-cooked meats appear to be highly atherogenic; whereas, boiled meats or boiled eggs do not seem to be. This still needs additional research, but I’ve been recommending to people that if you’re going to eat meat, then emphasize the gentlest form of cooking. As an example, a comparison of grilled and fried chicken, contained 9 times the amount of the advanced glycation end-products as when it’s boiled. So, use low-heat cooking and use in the presence of moisture and you will risk accumulating far fewer of the atherogenic effects than you would from frying, grilling and other high temperature methods.

Also, the effect of refined sugar has been overlooked in conventional medicine, at least. Eating large amounts of refined sugar reads like the Who’s Who of atherogenic blood profile… it raises triglycerides, promotes platelet aggregation in approximately 1/3 of the population, causes fasting hyper-insulinemia which is synonymous with insulin resistance, lowers HDL cholesterol levels… sugar does all of those things. There is an epidemiological association over the past century and a half between increased incidence of sugar intake and increase of cardiovascular disease.

Another that is overlooked is chlorinated water. You don’t hear about that much. We go out of our way to take 12,000 different types of antioxidants and then we consume huge amounts of a liquid every day that contains a powerful pro-oxidant – chlorine.

One editorialist wrote in the American Heart Journal as far back as 1965 that there were no countries in the world that have a high incidence of heart disease that do not chlorinate their water. It’s very easy to get the chlorine out…you can boil it or use a pinch of vitamin C in it or use water that is not chlorinated. There are other methods of getting rid of bacteria, for example ozonation or just using spring water that doesn’t contain chlorine.

Of course, the obvious that we all know…maintain proper body weight, don’t consume trans-fatty acids.

FRUCTOSE VERSUS SUCROSE?
There is a big debate in the alternative medicine community. I wrote a review article around 2002 (see references) – Adverse effects of dietary fructose…The very large amounts of free fructose that we consume from high fructose corn syrup is contributing to the epidemics of obesity, Diabetes type 2, and non-alcoholic fatty liver disease. Free fructose is absorbed more rapidly than fructose that has to be hydrolyzed from sucrose. In addition, the human body was not designed to consume such enormous amounts of fructose. Small amounts that we get in fruits and vegetables are probably fine but the 60 to 80 pounds per year from HFCS from an epidemiological standpoint since it coincides with the increasing prevalence of those three diseases. Drinks are the culprits. That ‘Super-Size Me’ movie about McDonalds, when his liver enzymes went off the chart – they said from all the fat, but they probably didn’t realize it was from the HFCS in the super-sized drinks as well… there is no evidence that high saturated fats causes fatty-liver disease but there is evidence that fructose does.

C-REACTIVE PROTEIN (CRP)
This is an inflammatory mediator; and, as you know, inflammation is one of the factors leading to the development of atherosclerosis and many other conditions as well…so we are looking for ways to lower CRP. One of the reasons it appears that the statin drugs lower the incidence of cardiovascular disease in high risk patients is not so much that it lowers serum cholesterol, but that lowers inflammation as demonstrated by a reduction in CRP. There are some allegations of fraud – the Jupiter study where they did some C-reactive protein work, but there is some support for the notion that the beneficial effect of statin drugs is due more to reduce the inflammatory effect than the cholesterol-lowering effects.

Furthermore, CRP is an independent risk factor for atherosclerosis…which means after you correct for body weight, serum cholesterol, etc. it remains as the predictor. So if we can find safe and helpful ways to lower CRP levels, then maybe we’ll be getting somewhere. And that brings us right back to the idea of the harsh cooking methods. The same cooking methods I mentioned before that don’t produce the AGEs, boiling and poaching, and eating a lot of raw foods which eliminates the concern about cooking methods, but if we are going to cook, use the gentler cooking technique.

They did a study of Type 2 diabetics and they ate the same or mostly the same foods and differed only in the methods of cooking and one set had twice as many AGEs as the other type of food and the CRP level was 65% higher with the high-AGEs diet than with the low-AGEs diet.

So if you want to reduce someone’s cardiovascular risk, it would seem that the cooking method is extremely important. There are some nutrients that have been looked at…magnesium might lower CRPand Vitamin C but that’s not as well worked out as with the cooking study.

Grilling – remember when the fire comes in contact with the food, that’s actually the harshest method you can imagine. That’s direct contact; you want to have the flame not touching the food. You may want to look up The Safe Grill on the Internet. It is designed to prevent the hottest portion of the flame from touching the food.

HOMOCYSTEINE
Back in the late ‘70’s Dr. Kilmer McCully broke with tradition and got himself in some academic hot water by claiming that homocysteine was not only a risk factor but a cause of cardiovascular disease. Homocysteine is a normal metabolite of methionine but it appears to be toxic. The human body has three different chemical pathways to get rid of homocysteine. One is to convert back to methionine; actually there are two different pathways to convert back to methionine and then, a third pathway where it is broken down by vitamin B6.

When you inject homocysteine into animals, you can induce atherosclerosis. When you look at people with a rare genetic condition known as homozygous homocysteinuria where they have two defective genes and can’t metabolize homocysteine properly, they develop atherosclerosis and osteoporosis by the age of 20. People that have the genetic polymorphisms which are much more gentle than the severe genetic disease, also have an increased risk of a wide range of conditions: atherosclerosis, infertility, recurrent miscarriage, dementia, and osteoporosis and others as well. There is some suggestion from the observational studies that this is causal because not only is homocysteine elevation itself associated with these diseases, but the genetic polymorphisms which lead to homocysteine elevations are also associated with an increased incidence. So if you can show a genetic factor, it is much more convincing than to show an association through observation out in the community for which there are always confounding factors. There aren’t really confounding factors for genetics.

So with that said, the evidence looking strong up to now – then you look at the controlled clinical trials. There are a few that showed that homocysteine lowering reverses atherosclerosis in the carotid arteries and a few that showed reduction in cardiovascular endpoints but the majority of the cardiovascular studies showed no benefit at all and occasionally, an adverse effect. In addition, there have been some studies indicating there is no benefit for the prevention of some of the other conditions associated with homocysteine when you take these B vitamins.

So there are some potential explanations for the conflicting results. As we all know, nutrients work in the body as a team as Roger Williams said and if you just take two or three nutrients our of the 40 to 60 that we know to be essential, the possibility of imbalances must be considered. There is some anecdotal evidence from a Adele Davis that if you take vitamin B6 alone that it depletes magnesium. She found that kids that took vitamin B6 became irritable, had insomnia and wet the bed and if they took magnesium with the B6, they didn’t get that. So based on that anecdote and also the fact that at least a half-dozen conditions for which magnesium is beneficial, vitamin B6 is also beneficial, and vice versa. So it appears these two nutrients work together in the body and taking only one, might deplete the other.

Magnesium deficiency is a substantially important factor in the development of cardiovascular disease. One theory is just taking a few vitamins causes imbalances with magnesium and then a beneficial effect of lowering homocysteine might be counterbalanced by an adverse effect of depleting magnesium. I don’t know if that’s true, but it certainly is plausible.

Another factor when looking at homocysteine, we are typically measuring fasting homocysteine levels. And folic acid, B6 and B12 which are the standard homocysteine lowering nutrients and are fairly effective but are less effective at lowering post-prandial homocysteine levels. Now if you think about it, we spend most of our life in the post-prandial state because by the time we get to be fasting 8 hours later or overnight fast, we have already eaten again. And some of us like me, are eating all day. So I think the peak homocysteine level may be a more important risk factor than the fasting homocysteine and there is some degree of experimental evidence to support that. The point of bringing this up is that the three nutrients mentioned are not particularly effective at preventing the post-prandial rise in homocysteine. Post prandial because when we consume protein which contains methionine, the methionine shoots up the homocysteine levels.

The two nutrients most effective at preventing post-prandial homocysteine level rise are betaine (trimethylglycine) and choline which are very closely related. There are studies showing as little as 500 mg a day of betaine, preferably more like a gram and a half a day. In some studies, they have used up to 6 grams or more and is fairly successful at preventing post-prandial or post-methionine load rises in homocysteine. So we need to go back and look to see whether taking betaine in addition to these other ones would benefit cardiovascular outcomes. If we do further homocysteine studies, everyone should get magnesium, and we should take betaine and/or choline along with the others. 500 mg daily of TMG would be sufficient to get some beneficial effect and there may be a greater effect with higher doses in some people.

If someone wants to lower homocysteine, they should take all of the nutrients we talked about… B6, B12, folate, betaine and if they want to add choline with it, that’s fine but the betaine has been better studied. When you use high doses of choline, you can end up smelling like rotten fish after a couple grams a day and that doesn’t seem to be the case with betaine. It gets broken down into trimethylamine which smells like dead, rotten fish but you have to be up in the 4 gram range unless you have some weak genetics so you can’t metabolize it very well so once you are up over a gram of choline a day …just warn your patients to watch out for that.

ARGININE
Arginine is a precursor to nitric oxide which is a vasodilator so if you want to Increase blood flow with a failing heart, or perhaps relieve angina by improving blood flow then arginine would be of theoretical value. It has been studied and been shown to improve quality of life in people with heart failure and to relieve angina. In some studies, it’s been shown to lower blood pressure but more negative than positive.

The main concern about arginine is in a study of MI survivors who were randomly assigned to take arginine (either 6 or 9 grams a day). They were followed for 6 months and there were 6 deaths in the arginine group and no deaths in the placebo group. So, this was statistically significant. Death was not an a priori endpoint which means they did a post hoc analysis and therefore it is possible that the increased death rate was due to chance. However that’s the only study that looked at death as an endpoint so it just stands out there and creates some concern.

As we know arginine is good for erectile dysfunction. Two of the men were found dead on their floor. They didn’t mention if they had a smile on their face …but with that said and for that reason, I don’t put arginine in my top therapies. We’ve got other therapies that are successful for these conditions but I would consider arginine for circumstances where the other don’t work well enough. I’ve come up with a hypothesis why arginine might have caused this problem…if in fact it did…we don’t know for sure.

As we’ve been talking about, high doses of a nutrient might cause imbalances with other ones. With respect to nitric oxide, which is a metabolite of arginine, although it is a vasodilator, it is also an unstable molecule that leads to the formation of reactive oxidants such as peroxynitrate. Peroxynitrate is not a well-known oxidant but it is one of the well known ‘nitrogen-derived oxidizing agent’ and it forms nitrogen-derived free radicals that promote inflammation and atherosclerosis. So it’s just like oxygen…oxygen is necessary for life and it is also toxic which is why we have all those antioxidants. So we also need a defense against nitrogen-derived free-radicals and it turns out from combing through the literature, what I found is that what seems to be the most important de-toxifier of reactive nitrogen species is… Gamma tocopherol! Back to what we were discussing before. So in the process of quenching nitric-oxide-derived oxidants, Gamma tocopherol is inactivated and, apparently, permanently. So to postulate… if you need arginine for some purpose, if you take mixed tocopherols along with it, if there is in fact an adverse effect on CV mortality, then mixed tocopherols might prevent that. This is an area where it would be very interesting to learn more.

Discussion with moderator about Viagra in a person with blockage..may not be such a good thing?…
Gaby: Well, people make their own collateral circulation which is too small to be seen on angiograms on catherization studies and vasodilation even in the face of what looks like 100% blockage might be clinically beneficial. That’s something in Chapt. 75 in my book – there are 342 chapters…75 is on atherosclerosis and ischemic heart disease and it presents information suggesting that blockages in some circumstances may not be the primary cause of mortality in MI’s - because it’s like a sponge, there are all these tiny collateral circulations that are too small to see but they are there and in fact it may be metabolic dysfunction at the cellular level rather than a lack of blood flow that’s a major factor, and if it is cellular dysfunction, nutrients that promote mitochondrial function like magnesium, carnitine, CoQ10 may be more important than we realize.

Moderator: the body always seems to find a way to get collateral circulation..think about stripping leg veins, or left bundle branch block, right bundle branch block; the body seems to figure out a way to get communications or blood to flow another way.

Moderator: So…Arginine might deplete Gamma Tocopherol?…
Gaby: I said ‘hypothetical’ about 10 times here. Yes… but the research is on such high doses of arginine…like 10 grams Gaby – but the average diet contains about 5 or 6 grams so it’s really not that huge.

CONGESTIVE HEART FAILURE:
Co Q10 and magnesium are the most important. Co Q is the best researched and, as you know, it is a component of the electron transport chain and is required for the synthesis of ATP. They’ve done studies of CoQ10 levels from cardiac biopsies of people with heart failure and I don’t know how they got a control group, but they did and the CoQ10 levels in myocardial tissue were significantly lower in heart failure patients and then when they supplemented them orally, they brought the CoQ10 levels up in the heart tissue. There have been numerous studies showing an increase in left ventricular ejection fraction and an increase in survival time, improvement of quality of life, and reduction in the New York Heart Association classification which results in improved which results in quality of life. There are at least 15 maybe 20 studies that have shown that most have been uncontrolled trials and two studies coming out of universities where the results were negative. One was at the U of Maryland where I went to medical school and I think they were treating a lot of inner city, indigent, poor, alcoholic, mal-nourished people who were on lasix and likely had magnesium deficiency for a bunch of different reasons and so since the nutrients work as a team, you are not going to expect CoQ10 to help someone who has moderately severe magnesium deficiency as well. So it gets back to the idea that you can’t expect a single nutrient to work in a debilitated, malnourished person.

Another possibility is that CoQ10 works more for diastolic heart failure than it does for systolic. Diastolic heart failure is not as well recognized but it comprises as much as 50% or more of people with heart failure. The better known is systolic heart failure and that’s where the left ventricle is not strong enough to pump out the blood with each systole so the ejection fraction or percentage of blood ejected with each pumping is diminished…and that’s the well-known form.

The lesser known form but apparently common, is diastolic dysfunction where the ventricle is impaired in some way so that it does not relax during the diastole and therefore not enough blood gets into the heart. So even if the percentage ejected may be sufficient, the amount of blood that gets into the heart to be pumped is not sufficient. There are virtually no clinical trials on drugs or anything else to treat diastolic heart failure. But one study in people with normal but impending diastolic heart failure showed that CoQ10 had some beneficial effect. In addition, potassium might be useful for diastolic heart failure.

So the bottom line about the CoQ10 is there are numerous studies that show benefit; some that don’t show benefit; but, the bulk of the evidence shows that it’s useful. A European study with double-blind placebo controlled trial with about 600 patients randomized to receive 150 mg of CoQ10 a day or placebo for one year found that during that time, there were 38% fewer hospitalizations for heart failure in the CoQ10 group than in the placebo group and this was highly statistically significant.

With magnesium, when you get to the heart failure stage or rather than being at risk of heart failure, you probably need intra-muscular or IV magnesium to get the best results. There may be a small benefit with oral magnesium. I’ve seen some dramatic results over the years with heart failure patients using IV magnesium as a component of the “Myers Cocktail”. I would use magnesium, B vitamins and low-dose vitamin C…all as a slow push. I’ve seen some amazing reversals in severe heart failure.

I also like carnitine and taurine and certainly we can’t forget good old thiamine which we tend to forget. Thiamine deficiency causes beriberi which leads to heart failure and loop diuretics like lasix deplete thiamine. There is some evidence that people with heart failure are frequently low in thiamine and if you supplement them it improves their heart function. So those are the main ones for the heart.

MITRAL VALVE PROLAPSE…MISSING SIMILAR NUTRIENTS?
That’s a quickie… 99% of it is magnesium deficiency. If you look at the clinical symptoms of magnesium deficiency: fatigue, anxiety, depression, chest pain, hyperventilation, insomnia, fears… all of those symptoms have been reported in MVP syndrome. There is some evidence that people with MVP have a higher than normal requirement for magnesium and it may be genetically determined.

A double blind study in the American Journal of Cardiology, of all places, they showed that about a 50% reduction in symptoms associated with MVP. It’s generally thought that the MVP itself does not improve but a magnesium expert in France, Dr. Durlach, who has stated on several occasions that you can reverse the actual physical prolapse after several years of therapy in about 20% of patients…so it is certainly worth long-term therapy.

There are a few case reports on using CoQ10 and carnitine but really very little other evidence so the mainstay there is the magnesium.
Moderator says she has MVP and the topical magnesium oil helps raise levels quickly along with the capsules and once in a while, IV.

Durlach thought there was a magnesium renal wasting syndrome; a renal leak and in severe cases when he couldn’t control symptoms with magnesium, he would give them potassium-sparing diuretics such as Triamterine or spironolactone which have the added effect of also preventing magnesium excretion.

Question on the Ubiquinol in patients with advanced congestive heart failure…Small study of 7 people…put them on very high doses (900 mg) of ubiquinone and plasma mcg/ test levels often were low at less than 2.5 mcg/ml and had limited clinical improvement. These patients were switched to ubiquinol and were given from 450 to 900 mg/day. They conclude the mean EF (ejection fraction) improved from 22% up to 39%. The ubiquinol absorption improved in people with severe heart failure. And the improvement in plasma CoQ levels is correlated with improve and measurement of left ventricular function. This was Langsjoen’s work.
Gaby: Langsjoen’s father was the first to be talking about CoQ for heart failure and he pretty much said exactly the same thing for ubiquinone probably 25 or 30 years ago

THYROID HORMONES… HYPOTHYROIDISM ON THE RISE?
If someone is truly hypothyroid and even if they are asymptomatic, there is some research showing that taking thyroid hormone will help prevent heart disease. Broda Barnes, MD, who was one of the proponents of treating people despite normal blood tests, said that the incidence of heart disease in his practice was 93% lower than predicted by the Framingham Study. He gave almost everyone thyroid hormones so I think that probably as much as 20% of the population, at least, has hypothyroidism and I’ve not found any nutrient therapies or diet changes that correct that. I’ve used low doses of thyroid hormone, typically desiccated thyroid – in the past, primarily Armour. There has been some problem with the recent formulation of Armour and I’m not sure what’s going on so I’m staying away from that and using Westhyroid or NatureThyroid from RLC Labs. That seems to work fine.

Gaby: They talk about asymptomatic people with clinical evidence of hypothyroidism. I did an interview for medical students just to demonstrate how I do my history and there was a 24-year-old medical student. I asked, do you suffer from fatigue and she said, No. I asked how many hours do you sleep? And she said 10. I asked what happens if you sleep 8 and she said, Oh, I’m exhausted. I then asked if she had dry skin… answer was No. I asked if she put cream on her legs, answer Yes. I asked what happens if you don’t and she said, oh, I have this horrible flakey skin. The next was about constipation…same thing.…she has to take fiber. So people have symptoms and they don’t even realize that they are symptoms…
(See references and article on Sub-laboratory Hypothyroidism…talks about diagnosing, treating, what to watch for.)


Q. EPA DHA in fish oils.ideal -- ratios for heart disease
A. Standard fish oil products contain about 18% EPA and about 12% DHA but it varies from product to product. There are probably 500 studies, both observational and clinical trials using fish oil or seeing how much fish people consume and I don’t think at this point there is any way of knowing what the optimal ratio is so I just go with 18:12 and if someone comes up with better research that says that the DHA is more important – then I would go with that but I haven’t seen any thing that would cause me to recommend an altered ratio at this point.

Q. Raising of HDL other than niacin?
A. Magnesium may raise, to some extent; also vitamin C may raise to some extent. And of course, drinking alcohol, but there is no clear evidence that raising HDL is going to reduce the funeral rate. We have all these observational studies where we see A associated with B, but we don’t have any proof that altering A necessarily alters B and that is true with HDL cholesterol. So at the very least, I think we should do things that are expected not to be harmful.

Exercise raises HDL; drinking alcohol has not been shown definitively, in my opinion, to prevent heart disease although it might turn out to be that way. It may just be that people who don’t drink have different biochemistry than drinkers and the difference is in the biochemistry rather than the fact that they drink that causes the change. But as you know, you can raise HDL with alcohol.

Q In hypertension, have you found you can control it enough with using just the nutrient-based diet approach?
A. It varies. Sometimes you can – probably about half the time. If you have someone who is overweight and not exercising, drinking coffee etc. I saw a guy who drank 20 cups of coffee a day and he was on two drugs. He stopped the coffee and didn’t need the medication. The person of normal body weight who seems to be eating a reasonable diet, that’s a more difficult. But 100 mg CoQ10 for a few months has been reported to lower blood pressure by as much as 15 over 10 in some cases It is highly variable. Some people respond to thyroid medication; other people who have food allergies as the major cause of their hypertension when they eliminate those foods, a couple days their Bp is normal. I always try to treat them – with a DASH type diet –high potassium, high fiber, moderate dairy products, nuts and seeds-- is worth a try.

End of Interview
Courtesy of
Designs for Health - "Science First"
Suffield, CT

REFERENCES
Nutrition in Medicine – Textbook by Alan R. Gaby, MD.
A Milestone in the History of 21st Century Medicine"
The result of thirty years of research by renowned authority on nutritional medicine
Nutritional Medicine is a textbook designed to teach healthcare practitioners how to use nutritional therapy as an alternative or adjunct to conventional medicine. Although the book is written for practitioners, it is also useful for educated members of the lay public who would like to be well informed regarding nutritional options for preventing and treating various health concerns.

Nutritional Medicine discusses more than 400 different health conditions and disorders. It also contains 60 chapters on individual nutrients (i.e., vitamins, minerals, amino acids, and other therapeutic agents) including biochemical effects, clinical indications, signs and symptoms of deficiency, adverse effects, drug interactions, nutrient interactions, and dosage and administration. Chapters on fundamentals of nutritional medicine (including dietary fundamentals, food additives, reactive hypoglycemia, food allergy, "sub-laboratory" hypothyroidism, and candidiasis) are also included.
With more than 900,000 words (about 11 times the size of an average-size book) and over 15,000 references to the scientific literature, Nutritional Medicine is a foundational cornerstone and should be on the desk of every healthcare practitioner.
[www.doctorgaby.com]

Gaby AR, Adverse effects of dietary fructose,
[www.ncbi.nlm.nih.gov]

Gaby AR. Sub-laboratory hypothyroidism and the empirical use of Armour thyroid.
[www.ncbi.nlm.nih.gov]

Complete list of Dr. Gaby’s Pub Med publications
[www.ncbi.nlm.nih.gov]

Thank You!!! Fascinating!!!