Is there something fishy about fish oil?

To be sure, there's plenty of misinformation out there about fish oil. Take a look at the swill that passes for health information on Woman's Day: On Call with Dr. Sandy: Fish Oil and Mercury:



Reader Question: My doctor recommended that I take a fish oil supplement, but I'm concerned about mercury. Is there any way to tell which brands are lowest in mercury content?



On Call Response: When it comes to OTC supplements, the answer is no. Though most fish oil supplements sold by major brands are probably safe, there's really no way to tell what's in the bottle or how much mercury it might contain.




Perhaps Dr. Sandy should read the many independent analyses performed on nutritional supplement fish oil, including those at Consumer Lab and Consumer Report before she offers her blind criticisms.

Lovaza vs fish oil supplements?

Lovaza is the FDA-approved form of fish oil that is available only by prescription. It contains 842 mg of the omega-3 fatty acids, EPA and DHA, per capsule.

The FDA application for Lovaza is viewable here on the FDA website. Interestingly, while there is plenty of the usual regulatory gobbledy-gook about toxicology, dose escalation, and efficacy in the extensive documentation, there is little said about the issue of contamination.

In other words, critics of nutritional supplement fish oil harp on the possibility of contamination with mercury and pesticide residues, like dioxin and PCBs (polychlorinated biphenyls). Yet there is virtually nothing about these same issues in the FDA application for Lovaza.

Let's take a look at a sample over-the-counter fish oil product. Our friends at PharmaNutrients (a new Track Your Plaque partner for nutritional supplements) have a fish oil product called PharmaNutrients" Cardio. Here's an independent analysis of the Cardio product (per 1000 mg fish oil capsule):

EPA content: 566.1 mg
DHA content: 216.6 mg
(Total EPA + DHA 782.7 mg)

Cardio passed all tests for peroxides, PCBs, dioxin, furans, dioxin-like PCBs, and heavy metals (arsenic, cadmium, lead, mercury) using criteria at least 60% more stringent than European Commission (EC) standards (EC standard <2 picograms/gm for dioxins and furans, PharmaNutrients <1 picograms/gm; EC standard <10 picograms/gm for dioxin-like PCBs, PharmaNutrients <3 picograms/gm). PCBs levels in particular are less than 0.009 ppm, 90% below the industry-wide purity standard of 0.09 ppm. Likewise, mercury is >90% lower than European Commission standards.

In other words, this over-the-counter "pharmaceutical grade" fish oil has virtually nothing but omega-3 fatty acids.

Interestingly, the PharmaNutrients fish oil capsule also contains the third omega-3 fatty acid, docosapentaenoic acid (DPA), a neglected form that some authorities have proposed has superior cardiovascular protective properties over eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). If DPA is included in the analysis, PharmaNutrient's Cardio contains a total of 900 mg omega-3 fatty acids per capsule.

At some point, I'd like to see a head-to-head comparison not just on purity grounds, since I am convinced that high-quality products like Cardio can match or exceed the purity of prescription fish oil, but on efficacy in raising omega-3 blood levels, the omega-3 index. (The omega-3 index is a predictor of heart attack and sudden cardiac death--the higher, the better.) My prediction: High-quality fish oil supplements will match or exceed prescription fish oil.

More on blood sugar

Take any of the following foods:

One chicken breast
Quarter-pound ground beef
6 oz salmon steak
½ cup raw almonds
3 eggs scrambled in olive oil

How much is blood sugar increased by any item in the above list?

If you said virtually zero, you’re correct. Eat any of these foods, regardless of portion size, and blood sugar won’t change substantially. If you started with a blood sugar of, say, 90 mg/dl, 1-2 hours later it would be 90 mg/dl. It might go up or even down a few milligrams, but for all practical purposes it remains substantially unchanged.

How much is blood sugar increased by the foods in this list:

2 slices multigrain bread
1 whole wheat bagel
4 oz high-fiber breakfast cereal
2 whole grain pancakes, 2 oz maple syrup

The foods in this list are a different story from the first. Depending on your body weight, exercise habits, and other factors, a typical blood sugar response in an otherwise healthy non-diabetic person would be 120 mg/dl to 160 mg/dl. In someone with diabetes, it could easily exceed 200 mg/dl.

That isn’t good. Large blood sugar excursions to 140 mg/dl have been clearly associated with greater risk for heart attack, progression to diabetes, inflammatory responses, and other adverse health effects. In fact, blood sugars as low as 100 mg/dl after eating have been associated with increased cardiovascular risk.

Then why are the USDA, American Heart Association, the American Dietetic Association, and the American Diabetes Association telling us to eat more of the foods that shoot blood sugar up to such high levels? “Eat more healthy whole grains”?

To see how much the issue of exaggerated blood sugars after eating applies to you, a simple blood sugar check 1-2 hours after eating can show you. Either your doctor can have the test drawn or you can purchase your own inexpensive glucose meter (e.g., Walmart, Wagreens).

My prediction: You will be very surprised at blood sugar responses after common foods, including “healthy whole grains.” And, by the way, keeping blood sugar excursions to a minimum will facilitate weight loss.

Postprandial blood sugar: Almonds vs. whole wheat bread

Here's my postprandial (after-eating) blood glucose demonstration.



I tested raw almonds vs. 100% whole wheat bread, matched for calories. (Full nutritional composition below.)



Blood sugars:

Raw almonds

Start:

One-hour after eating:





2 slices 100% whole wheat bread

Start:

One-hour after eating:





100% whole wheat bread, 2 large slices

Water (g) 24.69

Energy (kcal) 158

Protein (g) 8.29

Fat, total (g) 2.14

Carbohydrate (g) 26.43

Sugars, total (g) 3.56

Fiber, total dietary (g) 4.4

Cholesterol (mg) 0

Saturated fatty acids, total (g) 0.478

Monounsaturated fatty acids, total (g) 1.022

Polyunsaturated fatty acids, total (g) 0.384





23 almonds, raw



Energy (kcal) 159

Protein (g) 5.86

Fat, total (g) 13.64

Carbohydrate (g) 5.98

Sugars, total (g) 1.07

Fiber, total dietary (g) 3.4

Cholesterol (mg) 0

Saturated fatty acids, total (g) 1.03

Monounsaturated fatty acids, total (g) 8.525

Polyunsaturated fatty acids, total (g) 3.331



To get low-carb right, you need to check blood sugars

Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.

Food sources of vitamin K2: Reprint

For some reason, my December, 2007, Heart Scan Blog post, Food sources of vitamin K2, has been receiving a lot of traffic.

I therefore reprint the vitamin K2 post below.





Vitamin K2 is emerging as an exciting player in the control and possible regression of coronary atherosclerotic plaque. Only about 10% of dietary vitamin K intake is in the K2 form, the other 90% being the more common K1.

The ideal source of K2 is natto, the unpalatable, gooey, slimy mass of fermented soybeans that Japanese eat and has been held responsible for substantial decreases in osteoporosis and bone fractures of aging. Natto has an ammonia-like bouquet, in addition to its phlegmy consistency that makes it virtually inedible to anyone but native Japanese.

I say that the conversation on vitamin K2 is emerging because of a number of uncertainties: What form of vitamin K2 is best (so-called MK-4 vs. MK7 vs. MK-9, all of which vary in structure and duration of action in human blood)? What dose is required for bone benefits vs. other benefits outside of bone health? Why would humans have developed a need for a nutrient that is created through fermentation with only small quantities in meats and other non-fermented foods?

Much of the developing research on vit K2 is coming from the laboratories of Drs. Vermeer, Geleijnse, and Schurgers at the University of Maastricht in the Netherlands, along with several laboratories in Japan, the champions of K2.

MK-7 and MK-8,9,10 come from bacterial fermentation, whether in natto, cheese, or in your intestinal tract; MK-4 is naturally synthesized by animals from vitamin K1. While natto is the richest source of the MK-7 form, egg yolks and fermented cheeses are the richest sources of the MK-4 form.

Chicken contains about 8 mcg MK-4 per 3 1/2 oz serving; beef contains about 1 mcg. Egg yolks contain 31 mcg MK-4 per 3 1/2 oz serving (app. 6 raw yolks). Hard cheeses contain about 5 mcg MK-4 per 3 1/2 oz serving, about 70 mcg of MK-8,9; soft cheeses contain about 30% less. Natto contains about 1000 mcg of MK-7, 84 mcg MK-8, and no MK-4 per 3 1/2 oz serving.















Feta cheese

Thanks to the research efforts of the Dutch and Japanese groups, several phenomena surrounding vitamin K2 are clear, even well-established fact:

--Vitamin K2 supplementation (via frequent natto consumption or pharmaceutical doses of K2) substantially improves bone health. While K2 by itself exerts significant bone density/strength increasing properties in dozens of studies, when combined with other bone health-promoting agents (e.g., vitamin D3, prescription drugs like Fosamax and calcitonin), an exaggerated synergy of bone health-promoting effects develop.



--The MK-4 form of vitamin K2 is short-lived, lasting only 3-4 hours in the body. The MK-7 form, in contrast, the form in natto, lasts several days. MK-7 and MK-8-10 are extremely well absorbed, virtually complete.

--Bone health benefits have been shown for both the MK-7 and MK-4 forms.

--Coumadin (warfarin) blocks all forms of vitamin K.





Interestingly, farm-raised meats and eggs do not differ from factory farm-raised foods in K2 content. (But please do not regard this as an endorsement of factory farm foods.)

Another interesting fact: Since mammals synthesize a small quantity of Vit K2 forms from vitamin K1, then eating lots of green vegetables should provide substrate for some quantity of K2 conversion. However, work by Schurgers et al have shown that K1 absorption is poor, no more than 10%, but increases significantly when vegetables are eaten in the presence of oils. (Thus arguing that oils are meant to be part of the human diet. Does your olive oil or oil-based salad dressing represent fulfillment of some subconscious biologic imperative?)

If we believe the data of the Rotterdam Heart Study, then a threshold of 32.7 micrograms of K2 from cheese yields the reduction in cardiovascular events and aortic calcification.

It's all very, very interesting. My prediction is that abnormal (pathologic) calcium deposition will prove to be a basic process that parallels atherosclerotic plaque growth, and that manipulation of phenomena that impact on calcium depostion also impact on atherosclerotic plaque growth. Vitamins D3 and K2 provide potential potent means of at least partially normalizing these processes.

As the data matures, I am going to enjoy my gouda, Emmenthaler, Gruyere, and feta cheeses, along with a few egg yolks. I'm going to be certain to include healthy oils like olive and canola with my vegetables.


All images courtesy Wikipedia.

Copyright 2007 William Davis, MD

Family lessons

Lou was recovering from his 3rd bypass operation. This third go-round left him weaker, slower, less quick on the rebound. In fact, he was lucky to have survived.

At 71 years old, Lou went a good 15 years since his second bypass, another 10 years prior to his first bypass at age 46.

In the days immediately following Lou's bypass, I had a chance to talk to his son, who stayed at his Dad's bedside while Lou struggled through post-op recovery.

"Did your Dad tell you about why this has happened, what caused his heart disease?" I asked.

"Sort of. He just said I should get checked," Lou's son, Aaron, replied.

"Did he mention the lipoprotein(a) pattern he has?"

"No. He never mentioned anything like that. He just said to get checked."

That's how it gets played out more often than not: Mom or Dad has a heart attack, stents, or (3rd) bypass, the children are told to get checked. Getting "checked" assumes that the doctor knows what to check for.

In Lou's case, the reason why he was in the hospital getting his 3rd (and final) bypass was lipoprotein(a), along with genetically-determined small LDL particles, low HDL, a postprandial (after-eating) disorder, hypertension, and borderline diabetes, not to mention vitamin D deficiency, omega-3 fatty acid deficiency, and marginal thyroid function. (Lou, a retired city employee, had showed only marginal interest in correcting these patterns. While he accepted medications, he proved unwilling to engage in the diet and nutritional supplement strategies required to correct his patterns.)

So Lou's 3rd bypass operation provided a moment of reflection for Aaron to ask: "Could I share the fate of my Dad?" With Lou's combination of genetic patterns, there was at least a 75% likelihood that he did. Sadly, going to his doctor would likely yield little more than a cholesterol panel, a question about smoking, and a prescription for Lipitor.

Just getting "checked" would be, more than likely, a recipe for disaster for Aaron: heart disease in his 40s or 50s. That's why you need to take control over this sad state of affairs and ask--no, insist--that an effort be made to determine whether you might share your parents' fate.

Look like Jimmy Stewart


"This diet works great," Don declared. "But I think I've lost too much weight."

At 67 years old and 5 ft. 11 inches, Don began the program weighing 228 lbs (BMI 31.9). Because of high triglycerides, high blood sugar, high c-reactive protein, and excessive small LDL, I instructed Don to eliminate all wheat products from his diet, along with cornstarch and sweets. His intake of lean meats, eggs, vegetables, oils, raw nuts, etc. was unlimited.

Don now weighed 194 lbs, down 34 lbs over 6 months (BMI 27.1). Triglycerides, blood sugar, blood pressure, and well-being had improved dramatically; small LDL, however, had dropped only 30%--still room for improvement.

"My friends say I'm too skinny. They ask if I have cancer!"

I've heard this many times: Someone loses weight in a relatively short period of time and friends and family tell you you're too skinny. "It must be cancer. Nobody loses weight like that."

Unfortunately, many Americans have forgotten what normal looks like. Normal is certainly not a 190-lb, 5 ft 4 in woman, nor is it a 228 lb, 5 ft 11 inch man. But Americans have put on so much weight that the prevailing view of what constitutes "normal" weight has been revised upward. Normal is closer to what we see in old movies from the 1940s and '50s with people like Jimmy Stewart and Donna Reed. That's what we are supposed to look like.

So Don actually remains mildly overweight but is judged as "too skinny," or even cancer-ridden, by friends and family.

Ignore such comments. As you lose pounds and approach a truly desirable weight, realize that you are returning to the normal state, not the vision of "normal" now held by most Americans.

Getting vitamin D right

Vitamin D is, without a doubt, the most incredible "vitamin"/prohormone/neurosteroid I have ever encountered. Frankly, I don't know how we got anything accomplished in health pre-D.

Unfortunately, people I meet rarely take their vitamin D in a way that accomplishes full restoration of vitamin D blood levels. It really isn't that tough.

Here's a list of common tripping points with vitamin D:

"I take vitamin D: 1000 units a day."
This is probably the most common mistake I see: Taking a dose that is unlikely to yield a desirable blood level. (We use 60-70 ng/ml of 25-hydroxy vitamin D as our target.) Most men and women require 6000 units per day to achieve this level. There is substantial individual variation, however, with an occasional person needing much more, a rare person requiring as little as 1000 units.


"I bought some vitamin D on sale. They were white tablets."
Time and again, patients in my office who initially have had successful vitamin D replacement, despite being reminded that only oil-based forms should be taken, switch to tablets. While they initially showed a 25-hydroxy vitamin D blood level, for instance, of 67 ng/ml on 8000 units per day with an oil-based capsule, they switch to a tablet form and the next blood level is 25 ng/ml. In other words, tablets are very poorly or erratically absorbed.

I have had people use tablets successfully, however, by taking their vitamin D tablets with a teaspoon of oil, e.g., olive oil. Oil is necessary for full absorption.


"I'm going to Florida. I'll stop my vitamin D because I'm going to lay in the sun."
Wrong. 90% of adults over 40 years old have lost the majority of their ability to activate vitamin D in the skin. A typical response might be an increase in blood level from 25 to 35 ng/ml--a 10 ng increase with a dark brown tan.

There is an occasional person who, with sun exposure, increases blood levels substantially. This can occur in both fair-skinned and dark-skinned people, though I've never seen it happen in an African-American person. The occasional person who maintains the ability to convert vitamin D with sun exposure, or young people, should seasonally adjust their vitamin D dose, e.g., 6000 units winter, 3000 units summer, or some other regimen that maintains desirable blood levels. You can see that monitoring blood levels (we check levels every 6 months for the first 2 years) is crucial: You cannot know what your vitamin D needs are unless you assess 25-hydroxy vitamin D levels.


"I drink plenty of milk. I don't think I need to take vitamin D."
Oh, boy. This is so wrong on so many levels.

First of all, no adult should be drinking plenty of cow's milk. (A discussion for another day.) Second of all, cow's milk averages 70 units of vitamin D, often the D2 form (ergocalciferol), per 8 oz. Even if the FDA-mandated 100 units per day were present, an average adult dose of 6000 units would require 60 glasses of milk per day. Can you say "diarrhea"?

Likewise, other food sources of vitamin D, such as fish (300-400 units per serving) and egg yolks (20 units per yolk), are inadequate. This makes sense: Humans are not meant to obtain vitamin D from food, but from sun exposure over a large body surface area. And this is a phenomenon that is meant to occur only in the youthful, ensuring that nature takes its course and us older folks get old and make way for the young (i.e., unless we intervene by taking vitamin D supplements).


"My doctor said that my vitamin D blood level was fine. It was 32 ng/ml."

Let's face it: By necessity, your overworked primary care physician, who manages gout, hip arthritis, migraine headaches, stomach aches, prostate enlargement, H1N1, depression, etc., is an amateur at nearly everything, expert in nothing. Nobody can do it all and get it right. Likewise vitamin D. The uncertain primary care physician will simply follow the dictates of the laboratory form that specifies "30-100 ng/ml" as the "normal" or "reference range." Unfortunately, the laboratory often quotes population distributions of a lab measure, not an ideal or desirable level.

To illustrate the folly of population distributions of a measure, imagine you and I want to know what women weigh. We go to a local mall and weigh several thousand women. We tally up the results and find that women weigh 172 lbs +/- 25 lbs (the mean +/- 2 standard deviations). (That's true, by the way.) Is that desirable? Of course it isn't. Population average or population distribution does not necessarily mean ideal or desirable.


"My husband's doctor said he should take 4000 units per day. So I just take the same dose."
That would be fine if all adults required the same dose. However, individual needs can vary enormously. A dose that is grossly insufficient for one person may be excessive for another. Once again, vitamin D dose needs can be individualized by assessing 25-hydroxy vitamin levels in the blood.


"I don't need to take vitamin D. I already take fish oil."
I suspect this mistaken belief occurs either because people confuse fish oil with cod liver oil, which does contain some vitamin D. (Cod liver oil is not the best source of vitamin D, mostly because of the vitamin A content; also a discussion for another time), or because they've heard that eating fish provides vitamin D. However, fish oil capsules do not contain vitamin D unless it is added, in which case it should be prominently and explicitly stated on the label.


"I don't have to take vitamin D. It's summer."

For most people I know, if it's a bright, sunny July day, where are they likely to be? In an office, store, or home--NOT lying in the sun with a large body surface area exposed. Also, most people expose no more than 5-10% of surface area in public. I doubt you cut the grass in a bathing suit. Because of modern indoor lifestyles and fashion, the majority of adults need vitamin D supplementation year-round.


I advise everyone that gelcap vitamin D is preferable. Some, though not all, liquid drop forms have also worked. Take a dose that yields desirable blood levels. And blood levels of 25-hydroxy vitamin D are ideally checked every 6 months: in summer and in winter to provide feedback on how much sun activation of D you obtain.

If your doctor is unwilling or unable to perform vitamin D testing, fingerstick vitamin D test kits can be obtained from Track Your Plaque.

Jimmy Moore's thyroid adventure

My friend, Jimmy Moore of Living La Vida Low Carb, describes his thyroid experience here.

As Jimmy points out, he was looking for a way to jump-start a 50-lb weight loss. In my experience, low thyroid hormone levels ("hypothyroidism") are an exceptionally common cause for weight gain. Correcting even marginal hypothyroidism can facilitate weight loss, often resulting in 10 or more pounds of weight loss within the first month.

Unfortunately, Jimmy's thyroid hormone panel proved normal: TSH 1.3, thyroid hormones free T3 and free T4 in the mid- to upper-half of the reference range.

I say "unfortunately" because it is really an easy, inexpensive, and benign solution for losing weight. (I don't, of course, wish that Jimmy or anyone else develops a thyroid condition. But it really can provide gratifying weight loss results when thyroid function is low.) Jimmy might consider taking his oral temperature first thing in the morning as another means of assessing the adequacy of thyroid function.

Perhaps you will be luckier than Jimmy and have thyroid dysfunction that can be corrected and jump-start your weight loss program. Fingerstick thyroid test kits like the one Jimmy used are available here from Track Your Plaque.
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

  • Viagra Online

    9/22/2010 6:18:34 PM |

    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.

  • buy jeans

    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.

  • online pharmacy

    12/9/2010 6:03:19 AM |

    The proper diet is essential for diabetic treatment. It helps magically in patients suffering from diabetes. It provides relief from symptoms and various complications in diabetics. Many diabetic patients can control their blood glucose by losing weight and that is possible only be proper diet.

    Regards
    Alexa

Loading