What do Salmonella, E coli, and bread have in common?

Say you happen to eat some chicken fingers contaminated with bacteria because the 19-year old kid behind the counter failed to wash his hands after using the toilet, or because the kitchen is poorly managed with unwashed counters and cutting boards, or because the food is undercooked. You get a bout of diarrhea and cramps, along with a desire to banish chicken from your life.

Here's yet another odd wheat phenomenon: About 30% of people who eliminate wheat from their lives experience an acute food poisoning-like effect on re-exposure. You've been wheat-free for, say, 6 months. You've lost 25 lbs from your wheat belly, you've regained energy, joints feel better. You go to an office party where they're serving some really yummy looking bruschetta. Surely a couple won't hurt! Within a hour, you're getting that awful rumbling and unease that precede the explosion.

The majority of people who experience a wheat re-exposure syndrome will have diarrhea and cramps that can last from hours to days, similar to food poisoning. (Why? Why would a common food trigger a food poisoning-like effect? It happens too fast to attribute to inflammation.) Others experience asthma attacks, joint pains that last 48 hours to a week, mental fogginess, emotional distress, even rage (in males).

Wheat re-exposure in the susceptible provides a tidy demonstration of the effects of this peculiar product of genetic research. So if you are wheat-free but entertain an occasional indulgence, don't be surprised if you have to make a beeline to the toilet.

The world of intermediate carbohydrates

There are clear-cut bad carbohydrates: wheat, oats, cornstarch, and sucrose. (Fructose, too, but in a class of bad all its own.)

Wheat: The worst. Not only does wheat flour increase blood sugar higher than nearly all other carbohydrates, it invites celiac disease, neurologic impairment, mental and emotional effects, addictive (i.e., exorphin) effects, asthma, irritable bowel syndrome, acid reflux, sleepiness, sleep disruption, arthritis . . . just to name a few.

Oats: Yeah, yeah, I know: "Lowers cholesterol." But nobody told you that oats, including slow-cooked oatmeal, causes blood sugar to skyrocket.

Cornstarch: Like wheat, cornstarch flagrantly increases blood sugar.It also stimulates appetite. That's why food manufacturers put it in everything from soups to frozen dinners.

Sucrose: Not only does sucrose create a desire for more food, it is also 50% fructose, the peculiar sugar that makes us fat, increases small LDL particles, increases triglycerides, slows the metabolism of other foods, encourages diabetes, and causes more glycation than any other sugar.

But there are a large world of "other" natural carbohydrates that don't fall into the really bad category. This includes starchy beans like black, kidney, and pinto; rices such as white, brown, and wild; potatoes, including white, red, sweet, and yams; and fruits. It includes "alternative" grains like quinoa, spelt, triticale, amaranth, and barley.

For lack of a better term, I call these "intermediate" carbohydrates. They are not as bad as wheat, etc., but nor are they good. They will still increase blood glucose, small LDL, triglycerides, etc., just not as much as the worst carbohydrates.

The difference is relative. Say we compare the one-hour blood glucose effects of 1 cup of wheat flour product vs. one cup of quinoa. Typical blood sugar after wheat product: 180 mg/dl. Typical blood sugar after quinoa: 160 mg/dl--better but still pretty bad.

Some people are so carb-sensitive that they should avoid even these so-called intermediate carbohydrates. Others can have small indulgences, e.g., 1/2 cup, and not generate high blood sugars.

Heroin, Oxycontin, and a whole wheat bagel

For a substantial proportion of people who remove wheat from their diet, there is a distinct and unpleasant withdrawal syndrome. Here are the comments of Heart Scan Blog reader, Scott, from Texas:

Hello Dr. Davis,

I've been experimenting with diet, converging upon a Paleo type diet, but I keep running into problems. I have isolated the problem to cutting out wheat.

Sugar, rice, fruit, corn, potatoes, etc. are relatively ok to add or remove from the diet, but cutting out wheat in particular brings on a moderate headache with heavy fatigue all day long. This resembles the wheat withdrawal symptoms I found on your blog. As I write this, I'm on day 8 of wheat-free. I consume a fair variety of meat and veggies each day with a moderate amount of white rice for carbs. Perhaps a bowl of corn flakes with milk and half a bar of dark chocolate a day. I've learned from experience over the past 5 months or so that none of these foods affect the withdrawal. It's purely wheat.

My question is, what is the range of times for withdrawal symptoms that you've heard from different people? Has there been anyone who never recovered from the wheat withdrawal symptoms even after many months?

It's very tough to get work done like this, and even though my body and head feel much healthier in general, my sinuses have cleared, don't have to take a big nap after I eat, etc., I don't want to go down a path where this is the way things are going to be forever. 



People who have never experienced wheat withdrawal pooh-pooh the effect. But, for about 30% of people, wheat withdrawal is a real, palpable, and sometimes incapacitating experience.

Beyond removing an exceptionally digestible carbohydrate that yields blood sugar rises higher than nearly any other known food (due to the unique amylopectin structure of wheat-derived carbohydrate), wheat withdrawal is a form of opiate withdrawal, somewhat like stopping heroin, Oxycontin, and other opiates. Stop eating whole wheat toast for breakfast, whole grain sandwiches for lunch, or whole grain pasta for dinner, and the flow of exorphins, i.e., exogenous morphine-like compounds, stops. You experience dysphoria (sadness, unhappiness), mental "fog," inability to concentrate, fatigue, and decreased capacity to exercise. It is milder than withdrawal from prescription opiates. Unlike withdrawal from more powerful opiates like heroine, there are, thankfully, no seizures or hallucinations. There are also no deaths.

In my experience, most people get through with wheat withdrawal in about 5 days. An occasional person will struggle for as long as 4 weeks. Thankfully for Scott, I've never seen it last longer than 4 weeks. (Interestingly, people who survive the withdrawal syndrome are often prone to a peculiar re-exposure phenomenon that I will discuss in future, i.e., they get sick upon re-exposure.)

The modern dwarf mutant variant of Triticum aestivum (that our USDA urges us to eat more of) contains greater proportions of gluten proteins compared to wheat pre-1970; glutens are the source of wheat-derived exorphins.

Incidentally, a drug company should be releasing a drug in the next year that will contain naltrexone, an oral opiate blocking drug, for a weight loss indication. They claim it is a blocker of the "mesolimbic reward system." I say it's a blocker of wheat exorphins.

The five most powerful heart disease prevention strategies

You've seen such lists before: 5 steps to prevent heart disease or some such thing. These lists usually say things like "cut your saturated fat," eat a "balanced diet" (whatever the heck that means), exercise, and don't smoke.

I would offer a different list. You already know that smoking is a supremely idiotic habit, so I won't repeat that. Here are the 5 most important strategies I know of that help you prevent heart disease and heart attack:

1) Eliminate wheat from the diet--Provided you don't do something stupid, like allow M&M's, Coca Cola, and corn chips to dominate your diet, elimination of wheat is an enormously effective means to reduce small LDL particles, reduce triglycerides, increase HDL, reduce inflammatory measures like c-reactive protein, lose weight (inflammation-driving visceral fat), reduce blood sugar, and reduce blood pressure. I know of no other single dietary strategy that packs as much punch. This has become even more true over the past 20 years, ever since the dwarf variant of modern wheat has come to dominate.

2) Achieve a desirable 25-hydroxy vitamin D level--Contrary to the inane comments of the Institute of Medicine, vitamin D supplementation increases HDL, reduces small LDL, normalizes insulin and reduces blood sugar, reduces blood pressure, and exerts potent anti-inflammatory effects on c-reactive protein, matrix metalloproteinase, and other inflammmatory mediators. While we also have drugs that mimic some of these effects, vitamin D does so without side-effects.

3) Supplement omega-3 fatty acids from fish oil--Omega-3 fatty acids reduce triglycerides, accelerate postprandial (after-meal) clearance of lipoprotein byproducts like chylomicron remnants, and have a physical stabilizing effect on atherosclerotic plaque.

4) Normalize thyroid function--Start with obtaining sufficient iodine. Iodine is not optional; it is an essential trace mineral to maintain normal thyroid function, protect the thyroid from the hundreds of thyroid disrupters in our environment (e.g., perchlorates from fertilizer residues in produce), as well as other functions such as anti-bacterial effects. Thyroid dysfunction is epidemic; correction of subtle degrees of hypothyroidism reduces LDL, reduces triglycerides, reduces small LDL, facilitates weight loss, reduces blood pressure, normalizes endothelial responses, and reduces oxidized LDL particles.

5) Make exercise fun--Not just exercise for the sake of exercise, but physical activity or exercise for the sake of having a good time. It's the difference between resigning yourself to 30 minutes of torture and boredom on the treadmill versus engaging in an activity you enjoy and look forward to: go dancing, walk with a friend, organize a paintball tournament outdoors, Zumba class, plant a new garden, etc. It's a distinction that spells the difference between finding every excuse not to do it, compared to making time for it because you enjoy it.

Note what is not on the list: cut your fat, eat more "healthy whole grains," take a cholesterol drug, take aspirin. That's the list you'd follow if you feel your hospital needs your $100,000 contribution, otherwise known as coronary bypass surgery.

Topping up your vitamin D tank

Now that my vitamin D replacement experience dates back nearly 5 years, I've been witnessing an unusual phenomenon:

The longer you take vitamin D, the less you need.

Let me explain. You take 10,000 units D3 in gelcap form. 25-hydroxy vitamin D levels, checked every 6 months, have remained consistently between 60 and 70 ng/ml. Three years into your vitamin D experience and 25-hydroxy vitamin D level rises to 98 ng/ml--an apparent need for less vitamin D.

So we cut your intake from 10,000 units per day to 8000 units per day. Another 25-hydroxy vitamin D level 6 months later: 94 ng/ml. We cut dose again to 6000 units, followed by another 25-hydroxy vitamin D level of 66 ng/ml.

This has now happened in approximately 20% of the people who have been taking vitamin D for 3 or more years. I know of no formal analysis of this effect, what I call the "topping up" phenomenon. Reasoned simply, it seems to me that, once your vitamin D "tank" is topped up (i.e., tissue stores have been replenished), it requires less to keep it full.

No one has experienced any adverse consequence of this topping up effect though it has potential for some people to develop toxic levels if 25-hydroxy vitamin D levels are not monitored long-term. In my office, I measure 25-hydroxy vitamin D levels every 6 months.

It means that long-term monitoring of 25-hydroxy vitamin D is crucial to maintain favorable and safe levels.

Thirteen catheterizations later

When I first met her, Janet couldn't stop sobbing. She'd just been through her 10th heart catheterization in two years.

It started with chest pains at age 56, prompting her first heart catheterization that uncovered severe atherosclerotic blockages in all three coronary arteries. Her cardiologist advised a bypass operation.

Six months after the bypass operation, Janet was back with more chest pains, just as bad as before. Another heart catherization showed that two of the three bypass grafts had failed. The third bypass graft contained a severe blockage that required a stent, along with multiple stents in the two now unbypassed arteries.

In the ensuing 18 months, Janet returned for 8 additional catheterizations, each time leaving the hospital with one or more stents.

Janet's doctor was puzzled as to why her disease was progressing so aggressively despite Lipitor and the low-fat diet provided by the hospital dietitian. So he had Janet undergo lipoprotein testing (NMR):

LDL particle number: 3363 nmol/L
Small LDL particle number: 2865 nmol/L
HDL cholesterol: 32 mg/dl
Triglycerides: 344 mg/dl
Fasting blood glucose 118 mg/dl
HbA1c 5.8%

Unfortunately, Janet's doctor didn't understand what these values meant. He pretty much threw his arms up in frustration. That's when I met Janet.

From her lipoprotein panel and other values, it was clear to me that Janet was miserably carbohydrate-sensitive and carbohydrate-indulgent, as demonstrated by the extravagant quantity (2865 nmol/L) and proportion (2865/3363, or 85%) of small LDL, the form of LDL particles created by carbohydrate exposure. Janet struggled with depression over the years and had been using carbohydrate foods as "comfort" foods, often resorting to cookies, pies, cakes, breads, and other wheat-containing foods for emotional solace.

It took a bit of persuasion to convince Janet that it was low-fat, "healthy whole grains," as well as comfort foods, that had led her down this path. I also helped Janet correct her severe vitamin D deficiency, mild thyroid dysfunction, and lack of omega-3 fatty acids.

Since meeting Janet and instituting her new prevention program, she has undergone three additional catheterizations (performed by another cardiologist), all performed for chest pain symptoms that struck during periods of emotional stress. All showed . . . no significant blockage. (Apparently, the repeated "need" for stents triggered a Pavlovian response: chest pain = "need" for yet more stents.)

In short, correction of the causes of coronary atherosclerotic plaque--small LDL, vitamin D deficiency, omega-3 fatty acid deficiency, and thyroid dysfunction--and Janet's disease essentially ground to a halt.

Imagine, instead, that Janet had undergone 1) a heart scan to identify hidden coronary plaque 5-10 years before her first heart procedure, then 2) corrected the causes before they triggered symptoms and posed danger. She might have been spared an extraordinary amount of life crises, hospital procedures, expense (nearly $1 million), and emotional suffering.

High blood pressure vanquished

Heart Scan Blog reader, Eric, related his blood pressure success story to me:

I'm 34 and have been battling chronic hypertension (systolic 150-200, depending on my anxiety levels) even with multiple prescriptions for over a decade now. I've seen four different cardiologists, all stumped as to what is causing my hypertension. First, they suspected coarctation of my aorta [a constriction in the aorta], but an angiogram determined blood pressure readings were the same on both sides of the narrowing.

The second angiogram performed last year to determine if my coarct had worsened determined that it had not, but that my aorta had calcium build up. The cardiologist was stumped because he told me he hasn't seen calcium in a patient so young. Needless to say, this scared me to death, with my wife being pregnant with our first child. I asked if it could be reversed and he didn't know so he sent me to get a Berkeley lab.

The Berkeley came back with LDL 91, HDL 41, Triglycerides 73, CRP 4.1, vit D 26. The doctors weren't very knowledgeable about explaining to me what these meant and how I could correct the low vit D and high CRP. They told me to follow the low-fat diet recommended by Berkeley. Well I've already tried the DASH diet and didn't like how I felt or my energy levels, so I didn't transition.

I was at a loss until I encountered your blog and it was truly a gift. It was a refreshing feeling to meet a knowledgeable Dr. who knew what I was going through and seems to truly care about reversing calcium in the heart (something I never got from my any of my cardiologists). With your blog I have an appointment to get a heart scan here in CO and take that number along with my Berkeley results and join Track Your Plaque.

For the past 2 weeks I've been following your advice by taking a D3+K2 supplement with Omega3 Fish oil and avoiding all grain, wheat, sugar and I'm already down 4lbs to 223.5lbs at 6'5" tall and my blood pressure readings have been 128/54 and 129/60 the past 2 days! With your help I may not have the dark future my father had: dead at 48 with a massive heart attack.

Stay on the look out because I look forward to telling you how I'm one of your top calcium losers!

Eric, Colorado


Conventional medical care fails at so many levels for so many people. While Eric's doctors were busy contemplating the next angiogram, they were neglecting several crucial aspects of his health.

It's really not that tough. But it can mean doing the opposite of what conventional "wisdom" tell us.

DHEA and Lp(a)

DHEA supplementation is among my favorite ways to deal with the often-difficult lipoprotein(a), Lp(a).

DHEA is a testosterone-like adrenal hormone that declines with age, such that a typical 70-year old has blood levels around 10% that of a youthful person. DHEA is responsible for physical vigor, strength, libido, and stamina. It also keeps a lid on Lp(a).

While the effect is modest, DHEA is among the most consistent for obtaining reductions in Lp(a). A typical response would be a drop in Lp(a) from 200 nmol/L to 180 nmol/L, or 50 mg/dl to 42 mg/dl--not big responses, but very consistent responses. While there are plenty of non-responders to, say, testosterone (males), DHEA somehow escapes this inconsistency.

Rarely will DHEA be sufficient as a sole treatment for increased Lp(a), however. It is more helpful as an adjunct, e.g., to high-dose fish oil (now our number one strategy for Lp(a) control in the Track Your Plaque program), or niacin.

Because the "usual" 50 mg dose makes a lot of people bossy and aggressive, I now advise people to start with 10 mg. We then increase gradually over time to higher doses, provided the edginess and bossiness don't creep out.

The data documenting the Lp(a)-reducing effect of DHEA are limited, such as this University of Pennsylvania study, but in my real life experience in over 300 people with Lp(a), I can tell you it works.

And don't be scared by the horror stories of 10+ years ago when DHEA was thought to be a "fountain of youth," prompting some to take megadose DHEA of 1000-3000 mg per day. Like any hormone taken in supraphysiologic doses, weird stuff happens. In the case of DHEA, people become hyperaggressive, women grow mustaches and develop deep voices. DHEA doses used for Lp(a) are physiologic doses within the range ordinarily experienced by youthful humans.

No more cookies

Jeanne enjoyed her Christmas holidays. She especially liked sharing the cookies she made for her grandchildren, sneaking 2 or 3 every day over a couple of weeks. On top of this, she enjoyed the Christmas candy, egg nog, leftover stuffing and cranberry sauce, topped off with a night of nutritional debauchery on New Year's Eve.

Lipid panel in October:

Total cholesterol 146 mg/dl
LDL cholesterol 72 mg/dl
HDL cholesterol 64 mg/dl
Triglycerides 49 mg/dl

Lipid panel in early January:

Total cholesterol 229 mg/dl
LDL cholesterol 141 mg/dl
HDL cholesterol 59 mg/dl
Triglycerides 147 mg/dl


I call the holidays The Annual Wheat and Sugar Frenzy. It's the carbohydrates, especially those from products made of wheat and sucrose, that caused the marked shifts in Jeanne's lipid patterns. Let's take each parameter apart:

--Triglycerides go up due to de novo lipogenesis, liver conversion of carbohydrates into triglycerides. Triglycerides enter the bloodstream as VLDL particles which, in turn, interact with LDL and HDL.

--LDL goes up because carbohydrate exposure increases VLDL, followed by conversion to LDL. The triglyceride-rich LDL created is converted to small LDL particles. Had we measured small LDL changes in Jeanne, we likely would have measured something like an increase (by NMR) from 800 nmol/L to 1600 nmol/L, a carbohydrate effect.

--The increased VLDL also makes HDL triglyceride-rich, cause more rapid degradation of HDL particles. (It also makes them smaller, like LDL.) Given sufficient time (a few more months), HDL would drop into the 40's.

--Total cholesterol changes reflect the composite of the above numbers. (Total cholesterol = LDL cholesterol + HDL cholesterol + Trig/5) (Note that, as HDL drops, so will total cholesterol; that's why this value is worthless and should be ignored.)

So don't be surprised by the above distortions after a period of carbohydrate indulgence. Although your unwitting primary care doc will see such changes as opportunity for Lipitor, it is nothing more than the cascade of effects from a carbohydrate-driven distortion of lipoproteins.

How to become diabetic in 5 easy steps

If you would like to become diabetic in as short a time as possible, or if you have someone you don't like--ex-spouse, nasty neighbor, cranky mother-in-law--whose health you'd like to booby trap, then here's an easy-to-follow 5-step plan to make you or your target diabetic.


1) Cut your fat and eat healthy, whole grains--Yes, reduce satiety-inducing foods and replace the calories with appetite-increasing foods, such as whole grain bread, that skyrocket blood sugar higher than a candy bar.

2) Consume one or more servings of juice or soda per day--The fructose from the sucrose or high-fructose corn syrup will grow visceral fat and cultivate resistance to insulin.

3) Follow the Institute of Medicine's advice on vitamin D--Take no more than 600 units vitamin D per day. This will allow abnormal levels of insulin resistance to persist, driving up blood sugar, grow visceral fat, and allow abnormal inflammatory phenomena to persist.

4) Have a bowl of oatmeal or oat cereal every morning--Because oat products skyrocket blood sugar, the repeated high sugars will damage the pancreatic beta cells ("glucose toxicity"), eventually impairing pancreatic insulin production. (Entice your target even further: "Would you like a little honey with your oatmeal?") To make your diabetes-creating breakfast concoction even more effective, make the oatmeal using bottled water. Many popular bottled waters, like Coca Cola's Dasani or Pepsi's Aquafina, are filtered waters. This means they are devoid of magnesium, a mineral important for regulating insulin responses.

5) Take a diuretic (like hydrochlorothiazide, or HCTZ) or beta blocker (like metoprolol or atenolol) for blood pressure--Likelihood of diabetes increases 30% with these common blood pressure agents.

There you have it! Perhaps we should assemble a convenient do-it-yourself-at-home diabetes kit to help, complete with several servings of whole grain bread, a big bottle of cranberry juice, some 600 unit vitamin D tablets, a container of Irish oatmeal, and some nice bottled water.
Blame the niacin

Blame the niacin

Despite the fact that niacin is:

1) A vitamin--vitamin B3

2) One of the oldest cholesterol-reducing agents around with a long-standing track record of effectiveness and safety

3) Available as a prescription drug as well as a variety of "nutritional supplements"

most physicians remains shockingly unaware of its benefits, effects, and side-effects. Most, in fact, are either ignorant or frightened of advising their patients on niacin use. As a result, I commonly have to tell my patients to resume the niacin that their primary care physician has (wrongly) stopped because of itchy feet, grumpiness, groin rash, urinary tract infections, nightmares, diarrhea, hair loss, runny nose, etc. All of these are REAL reasons doctors have advised patients to stop niacin (though none were actually due to niacin).

Is niacin really that troublesome? No, it's not. In fact, if used properly, it's among the most effective and safe tools available for correction of low HDL, small LDL and other triglyceride-containing lipoproteins, lipoprotein(a), and dramatic reduction of heart attack risk. If added to a statin agent, the heart attack risk reduction can approach 90%.

Statins are just too easy for doctors to prescribe. Niacin, on the other hand, requires a good 15-20 minutes to describe how to use it. It could generate an occasional phone call from a patient who struggles with the annoying but largely harmless and temporary "hot-flush" feeling, a lot like a hot blush. Given a choice, most doctors would simply choose not to be bothered. For this reason, I'll commonly see many, many people with uncorrected low HDLs and other patterns.

Have a serious discussion and press for confident answers if you find your doctor reflexively telling you that the wart on your thumb should be blamed on niacin.

Here are the steps we advise that really make taking niacin easy and tolerable:

1) Take with dinner.

2) Take with 2 extra glasses of water. If you experience the hot-flush later on, drink an additional 2 8-12 oz glasses of water i.e., a total of 16-24 oz). Extra hydration is extremely effective for blocking the hot-flush.

3) Take a 325 mg, uncoated aspirin. This is only necessary in the beginning or with any increase in dose, rarely chronically for any length of time.


This is not to say that there aren't occasional people who are truly and genuinely intolerant to niacin. It does happen. But those people are a small minority, less than 5% of people in my experience. Niacin is far more effective and safe than most physicians would have you believe.

Comments (7) -

  • madcook

    10/31/2006 6:12:00 AM |

    I've taken prescription Niaspan for over an year and a half.  Several times I've had an unintended "untoward" reaction, more than a blush, more than a flush... more like a niacin storm!  Each time I've learned something new, however.  Yes, hydration is very important.  There are certain foods and drugs which apparently dam up the same metabolic pathway as niacin, and can cause a pretty nasty reaction.  Among these, at least for me, are certain long acting antibiotics (Zithromax), spicy chai tea, pepperoni (not supposed to go there anyway!) and very spicy foods, if taken near the time of Niaspan dosing.  I was advised by my Dr. that Benadryl syrup would help to shorten the duration of the "storm".  Mostly it's a case of dietary management and timing of dosage.  The good done by niacin certainly still outweighs the occasional bad side effects!

  • Jim

    3/14/2008 4:03:00 PM |

    Another comment about niacin from this long-time niacin user, maybe folks will find it useful...
    Dr. Davis's advice to hydrate heavily to prevent/reduce flushing is, alas, not completely effective. One can easily prove this for oneself. The next time you experience a big flush, consume as much water as you are able, and see if the flush quickly resides..does it?  No. Hydration is certainly great advice, I'm not knocking it, but as a flush reduction strategy, it isn't enough. One commentor here mentioned quercetin.  It seems some recent research on certain flavonoids (quercetin, luteolin) have produced good results,better than aspirin, which was mentioned in this thread.  One needs to experiment and see if supplements such as these do help, taken maybe 30-45 minutes before the niacin dose. I have some other comments on niacin strategies I've hardly seen mentioned anywhere, but I'll wait until (1) I see my posts are approved (I'm new here), and (2) that people are interested. Let's see if there is any feedback. Regards, Jim

  • mill

    6/27/2008 5:43:00 PM |

    I've been taking niacin  2 times daily for 6 months and dropped my cholestral from 240 to 162.  Can I go back to once daily?

  • Anonymous

    12/30/2008 10:15:00 PM |

    I have seen some research papers that report that NIACIN, Nicotinamide and/or SAMe ( maybe also other methyl donors such as TMG ) can cause Parkinson's disease. I wonder if niacin can be converted to Nicotinamide in the body. Please see their abstracts and URLs below. Thank you.



    Niacin Metabolism and Parkinson’s Disease

    Tetsuhito FUKUSHIMA1)
    1) Department of Hygiene & Preventive Medicine, Fukushima Medical University School of Medicine
    Abstract
    Epidemiological surveys suggest an important role for niacin in the causes of Parkinson’s disease, in that niacin deficiency, the nutritional condition that causes pellagra, appears to protect against Parkinson’s disease. Absorbed niacin is used in the synthesis of nicotinamide adenine dinucleotide (NAD) in the body, and in the metabolic process NAD releases nicotinamide by poly(ADP-ribosyl)ation, the activation of which has been reported to mediate 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s disease. Recently nicotinamide N-methyltransferase (EC2.1.1.1) activity has been discovered in the human brain, and the released nicotinamide may be methylated to 1-methylnicotinamide (MNA), via this enzyme, in the brain. A deficiency in mitochondrial NADH:ubiquinone oxidoreductase (complex I) activity is believed to be a critical factor in the development of Parkinson’s disease. MNA has been found to destroy several subunits of cerebral complex I, leading to the suggestion that MNA is concerned in the pathogenesis of Parkinson’s disease. Based on these findings, it is hypothesized that niacin is a causal substance in the development of Parkinson’s disease through the following processes: NAD produced from niacin releases nicotinamide via poly(ADP-ribosyl)ation, activated by the hydroxyl radical. Released excess nicotinamide is methylated to MNA in the cytoplasm, and superoxides formed by MNA via complex I destroy complex I subunits directly, or indirectly via mitochondrial DNA damage. Hereditary or environmental factors may cause acceleration of this cycle, resulting in neuronal death.

    Key words:
    nicotinamide N-methyltransferase, 1-methylnicotinamide, poly(ADP-ribosyl)ation, mitochondria, complex I

    Pasted from http://www.jstage.jst.go.jp/article/ehpm/10/1/10_3/_article


    Parkinson's disease: the first common neurological disease due to auto-intoxication?
    A.C. Williams1, L.S. Cartwright2 and D.B. Ramsden2
    From the Divisions of 1Neurosciences and 2Medical Sciences, University of Birmingham, Birmingham, UK
     
    Parkinson's disease may be a disease of autointoxication. N-methylated pyridines (e.g. MPP+) are well-established dopaminergic toxins, and the xenobiotic enzyme nicotinamide N-methyltransferase (NNMT) can convert pyridines such as 4-phenylpyridine into MPP+, using S-adenosyl methionine (SAM) as the methyl donor. NNMT has recently been shown to be present in the human brain, a necessity for neurotoxicity, because charged compounds cannot cross the blood-brain barrier. Moreover, it is present in increased concentration in parkinsonian brain. This increase may be part genetic predisposition, and part induction, by excessive exposure to its substrates (particularly nicotinamide) or stress. Elevated enzymic activity would increase MPP+-like compounds such as N-methyl nicotinamide at the same time as decreasing intraneuronal nicotinamide, a neuroprotectant at several levels, creating multiple hits, because Complex 1 would be poisoned and be starved of its major substrate NADH. Developing xenobiotic enzyme inhibitors of NNMT for individuals, or dietary modification for the whole population, could be an important change in thinking on primary and secondary prevention.


    Pasted from http://qjmed.oxfordjournals.org/cgi/content/full/98/3/215

    see also
    http://www.springerlink.com/content/d5wurtwylvpcy04q/


    But,on the contrary,the paper below seems to suggest that niacin protects from Parkinson's.

    Title: Does diet protect against Parkinson's disease? Part 4 – vitamins and minerals
    Author(s): Isabella Brown
    Journal: Nutrition & Food Science
    ISSN: 0034-6659
    Year: 2004 Volume: 34 Issue: 5 Page: 198 - 203
    DOI: 10.1108/00346650410560343
    Publisher: Emerald Group Publishing Limited
    Abstract: This paper is the fourth in a series on Parkinson's disease and diet and investigates the role which antioxidant vitamins A and C, niacin and selenium may have on the incidence of the disease. Oxidative stress is believed to be a key factor in the development of PD and all of these have a role in preventing oxidative stress mediated cell damage. Dietary information was obtained via questionnaires. Vitamin C was found to reduce the risk of PD by 40 per cent in one study, although this was not supported by other studies. Niacin was associated with an at least 70 per cent reduced risk of PD incidence in a number of studies. No evidence was found to support a role for vitamin A or selenium. There is a need for further research to support or disprove the roles of these antioxidant vitamins within the aetiology of PD.
    Keywords: Diet, Diseases, Lifestyles, Vitamins
    Article Type: Research paper
    Article URL: http://www.emeraldinsight.com/10.1108/00346650410560343

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    One of the ways to deal with coronary heart disease is by eating healthy there is no magical pill in this case, it's just as simple as that.

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    11/2/2010 7:48:20 PM |

    Have a serious discussion and press for confident answers if you find your doctor reflexively telling you that the wart on your thumb should be blamed on niacin.

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    Regards
    Alexa

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