Flush-free niacin kills

29. November 2008 William Davis (12)
Here, I re-post a conversation I've posted before, that of the scam product, "no-flush" niacin, also known as "flush-free" niacin.

I find this issue particularly bothersome, since I have a patient or two each and every week who forgets the explicit advice I gave them to avoid these scam products altogether. Despite costing more than conventional niacin, they exert no effect, beneficial or otherwise. Niacin--the real thing--exerts real and substantial beneficial effects. No-flush or flush-free does nothing except drain your wallet. I continue to marvel at the fact that supplement manufacturers persist in selling this product. Ironically, it commands a significant premium over other niacin forms.

They are outright scams that should be avoided altogether.


My former post, No-flush niacin kills:

Gwen was miserable and defeated.

No wonder. After a bypass operation failed just 12 months earlier with closure of 3 out of 4 bypass grafts, she has since undergone 9 heart catheterization procedures and received umpteen stents. She presented to me for an opinion on why she had such aggressive coronary disease (despite Lipitor).

No surprise, several new causes of heart disease were identified, including a very severe small LDL pattern: 100% of LDL particles were small.

Given her stormy procedural history, I urged Gwen to immediately drop all processed carbohydrates from her diet, including any food made from wheat or corn starch. (She and her husband were shocked by this, by the way, since she'd been urged repeatedly to increase her whole grains by the hospital dietitians.) I also urged her to begin to lose the 30 lbs of weight that she'd gained following the hospital dietitians' advice. She also added fish oil at a higher-than-usual dose.

I asked her to add niacin, among our most effective agents for reduction of small LDL particles, not to mention reduction of the likelihood of future cardiovascular events.

Although I instructed Gwen on where and how to obtain niacin, she went to a health food store and bought "no-flush niacin," or inositol hexaniacinate. She was curious why she experienced none of the hot flush I told her about.

When she came back to the office some weeks later to review her treatment program, she told me that chest pains had returned. On questioning her about what she had changed specifically, the problem became clear: She'd been taking no-flush niacin, rather than the Slo-Niacin I had recommended.

What is no-flush niacin? It is inositol hexaniacinate, a molecule that indeed carries six niacin molecules attached to an inositol backbone. Unfortunately, it exerts virtually no effect in humans. It is a scam. Though I love nutritional supplements in general, it pains me to know that supplement distributors and health food stores persist in selling this outright scam product that not only fails to exert any of the benefits of real niacin, it also puts people like Gwen in real danger because of its failure to provide the effects she needed.

So, if niacin saves lives, no-flush niacin in effect could kill you. Avoid this scam like the plague.

No-flush niacin does not work. Period.


Disclosure: I have no financial or other relationship with Upsher Smith, the manufacturer of Slo-Niacin.


Copyright 2008 William Davis, MD
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Comments (12) -

  • JPB

    11/29/2008 4:15:00 PM |

    What is your opinion of "Nia-Span"?  My former doctor insisted that this "by prescription only" drug was the only way to take niacin.  The cost per month was virtually the same as for a statin.  (BTW, I declined this product and continued with regular niacin.)

  • Anna

    11/29/2008 4:31:00 PM |

    FYI: the Slo-Niacin link isn't working.

  • Zbig

    11/29/2008 11:02:00 PM |

    RDA for niacin is 18 mg/day - what is your opinion on that, sir?
    BTW, do you guys in the States just go to a pharmacy and buy niacin and D3 without a prescription?

  • Anonymous

    11/30/2008 6:37:00 AM |

    "Slo-Niacin" uses a "polygel" to delay release of the nicotinic acid.  I've been taking Carlson's "Niacin-Time" (also nicotinic acid) which uses brazil wax to delay release.

    The Carlson's product is about a third the price of the Slo-Niacin.

  • IggyDalrymple

    12/1/2008 1:13:00 AM |

    I've been taking regular (not no-flush) niacin for a few months.  Dr Davis recommends "Slo-Niacin" but I got sick from taking timed-release niacin back in the 80s and "Slo-Niacin" sounds suspiciously like "Timed-Release".  I should know in January when I have bloodwork, if the regular niacin helps.

  • Anonymous

    12/3/2008 9:26:00 PM |

    JPB: Niaspan releases over 6-8 hours and yes..it is prescription only. I substituted it for Endur-acin which is MUCH cheaper and non-prescription and also releases over 6-8 hours. No difference in my lipid profiles...just big savings in my pocket book.

    Zbig: 18mg is probably sufficient as a RDA, but in order to achieve the lipid lowering affects from Niacin, one has to take larger doses of 500mg or more from what I understand. And yes, we can buy many supplements like (high dose) niacin, vitamin D3 & even DHEA without a prescription here in the USA.

    Anonymous: I believe Carlson buys their "Niacin-Time" from Endur. I looked at the picture on the Carlson website and the tablets are the exact same shape as Endur-acin. Endur has been around since the late 1980's from what I understand. You can buy direct from Endur.

    IggyDalrmple: Here is a link to an excellent article about (time-release) Niacin written by Doctor Davis himself:

    http://www.lef.org/magazine/mag2007/mar2007_atd_01.htm

  • CindynHouston

    2/3/2009 5:15:00 AM |

    Hi, Id like to know what research supports flush free Niacin has no effect on the human body ?
    I had/have horrible heart palpitations after a heart attack, and after taking Flush Free Niacin 2 to 3 times daily, control them, while time released I tried did not .. and Im afraid to take regular Niacin being so unstable.  I take several other things as well now, but not at the beginning.  I have Late Stage Lyme which has its own set of causal factors as well as the typical ones, but if it has no effect on the human body .. it wouldnt work period.  So, I would guess ..  like all else one thing might work for some, another substance for another depending on what I wish they would narrow down to "Cause".  I still have high Blood pressure, some medications work for a week or two, then stop being effective.  Areas of the brain control heart beat .. I have no clue if this is the whats causing high blood pressure or not .. Lyme can go any where and do anything .. Ive had it since I was a child with mild symptoms until my immune system got a faulty in mid thirties when it became aggressive.  No Doctors know how to treat other than antibiotics, dont treat symptoms like really bad hypercoagulation (thick blood) caused by being exposed to bacteria etc for a long period of time and the immune system becoming over active .. 2002 I had an attack which took me out almost completely .. No heart or other doctor even tried to diagnose and gave me a "hearts fine" .. 3 yrs later I had an almost deadly heart attack.  All these yrs, almost 10 .. spent trying to find help, treating symptoms on my own, having no family and absolutely No life, except for trying to survive. (people with Lyme ramble) Though its good to know info.... Question still remains about Flush Free Niacin...

  • Anonymous

    8/25/2009 9:29:49 PM |

    "IHN is more effective than niacin in its hypocholesterolemic,
    antihypertensive and lipotropic effects"
    Welsh AL, Eade M. Inositol hexanicotinate for improved nicotinic acid therapy.
    Int Record Med 1961;174:9-15.

    "significant lipid-lowering effects of IHN at doses of 400 mg 3-4 times daily"
    Dorner V, Fischer FW. The influence of m-inositol hexanicotinate ester on the serum lipids and lipoproteins. Arzneim-Forsch 1961;11:110-113.

    Sommer H. Nicotinic acid levels in the blood and fibrinolysis under the influence of the hexanicotinic ester of m-inositol. Arzneim Forsch. 1975;15:1337

    "IHN was found to be more effective than niacin in reducing hypercholesterolemia"
    El-Enein AMA, Hafez YS, Salem H, Abdel M. The role of nicotinic acid and inositol hexaniacinate as anticholesterolemic and antilipemic agents.
    Nutr Reports Int 1983;28:899-911.

    "Derivatives of niacin have been examined for their ability to alter lipid levels as well as niacin. It would be advantageous if the niacin vasodilation (flush) were eliminated or removed. The main disadvantage of the niacin derivatives will be cost. Inositol hexanicotinate is an ester of inositol and niacin. In the body it is slowly hydrolyzed releasing both of these important nutrients. The ester is more effective than niacin in lowering cholesterol and triglyceride levels, Abou El-Enein, Hafez, Salem and Abdel (1983). I have used this compound, Linodil, available in Canada but not the U.S.A. (at the time this paper was written) for thirty years for patients who can not or will not tolerate the flush. It is very gentle, effective, and can be tolerated by almost every person who uses it."
    From: Niacin, Coronary Disease and Longevity by Abram Hoffer, M.D., Ph.D.

  • LynP

    11/16/2009 5:25:16 AM |

    Question:  at dinner took 500 mgm Slo-Niacin and within a few hrs had some stomach unpleasant...sensations might be the best description, then my glucose rose.  Fasting rose 25 pts (shock) and yesterday was marked with ravenous hunger and 15-20 pts higher glucose all day; today's fasting was still higher than usual.  Is this expected?  It's almost as if it is undoing the work of my 1500 mg metformin ER in reducing the production of sugar in the liver. This isn't going to wk with higher glucose.  Suggestions? Comments?
    6/25/09 labs: TRI-119, calc LDL-150, HDL-57, D-35, TSH-4.5, AIC-6.4. Taking 12.5 mg Maxzide, 4K IU D3.
    9/22/09 labs: TRI-145, calc LDL-147, HDL-60, D-41, TSH-5.5, AIC-6.5, ApoB-111. Taking 12.5 mg Maxzide, 8K IU D3.
    Doc put me on 25 mcg levothyroxine (don't think this is enough or I need Armour).

    I think my TRI is up from too much carb (eat super low, ate a bit more more berries over summer).  I think my LDL is up from my rising TSH (free T4 & T3 midrange), been rising since Sept08 when it was 2.8 (when I started taking vit D). Wt loss (obese) has been stalled until I started subbing eggs for hi-protein shake with 2-3 ozs coconut milk a month ago.  TSH was high in 2001 (4.7) with high amts of reverse T3 (doc won't test for it)& given 2 mcg Cytomel but my TC was 205 with TRI=100. Now what to do?  Try the 250 mgm SloNiacin & see what happens?  Or just concentrate on improving D levels and improving thyroid function and hoping they help normalize lipids? Just looking for suggestions, not treatment, all ideas will be run by doc. He said statins or niacin...I'm female no familiy hist of heart probs, why statins with no good studies for women? 'Cause he takes a statin *sigh*.

  • Anonymous

    8/16/2010 3:17:08 AM |

    After my heart attack from Late Stage Lyme Disease causing hypercoagulation/thick blood .. after released from the hospital, I had/have severe heart palpatations .. and IM SORRY BUT, FLUSH FREE NIACIN DOES WORK!!  I have to take 2-500mg twice daily and it stops the heart palpatations .. its no gimmick or hype.  IT Works !!  Ive heard about the severe very uncomfortable flush rush with regular Niacin which I think would scare me and make me panick, if not make me ill with the fragile state my system is in.  Purchased at any store online or otherwise .. a lot less than and w/no side effects, I also take Argnine to help open my vessels, but is not needed to stop my heart palpatations. Obviously, something is wrong though if I or anyone is having heart palpatation, so you should keep looking or asking RN/head nurse until you find a heart doctor who will actually address the issue and find out whats going on!!  Once in a while with stressful event I do need to take a beta blocker to stop palpations, but only 3-5 times a yr.  NO SIDE EFFECTS like beta blockers...

  • buy jeans

    11/3/2010 3:18:31 PM |

    Given her stormy procedural history, I urged Gwen to immediately drop all processed carbohydrates from her diet, including any food made from wheat or corn starch. (She and her husband were shocked by this, by the way, since she'd been urged repeatedly to increase her whole grains by the hospital dietitians.) I also urged her to begin to lose the 30 lbs of weight that she'd gained following the hospital dietitians' advice. She also added fish oil at a higher-than-usual dose.

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You just THINK you're low-carb

27. February 2010 William Davis (72)
Systematically checking postprandial (after-eating) blood sugars is providing some great insights into crafting a better diet for many people.

I last discussed the concept of postprandial glucose checks in To get low-carb right, you need to check blood sugars.

Here are some important lessons that many people--NON-diabetic people, most with normal blood glucoses or just mildly increased--are learning:

Oatmeal yields high blood sugars. Even if your fasting blood sugar is 90 mg/dl, a bowl of oatmeal with skim milk, walnuts, and some berries will yield blood sugars of 150-200 mg/dl in many people.

Cheerios yields shocking blood sugars. 200+ mg/dl is not uncommon in non-diabetics. (Diabetics have 250-350 mg/dl.)

Fruits like apples and bananas increase blood sugar to 130 mg/dl or higher.

Odd symptoms, such as mental "fog," fatigue, and a fullness in the head, are often attributable to high blood sugars.

A subset of people with lipoprotein(a) can have wildly increased blood sugars despite their slender build and high aerobic exercise habits.


Once you identify the high blood sugar problem, you can do something about it. The best place to start is to reduce or eliminate the sugar-provoking food.

The LDL-Fructose Disconnect

26. February 2010 William Davis (8)
I believe that we can all agree that the commonly obtained Friedewald LDL cholesterol (what I call "fictitious" LDL cholesterol) is wildly inaccurate. 100%--yes, 100% inaccuracy--is not at all uncommon.

This flagrant inaccuracy, unacceptable in virtually every other discipline (imagine your airplane flight to New York lands in Pittsburgh--close enough, isn't it?), is highlighted in the University of California study by Stanhope et al I discussed previously.

32 participants consumed either a diet enriched with either fructose or glucose. Compared to the effect of glucose, after 10 weeks fructose:

Increased LDL cholesterol (calculated) by 7.6%

Increased Apoprotein B (a measure of the number of LDL particles) by 24%

Increased small dense LDL by 41%

Increased oxidized LDL by 12.6%


In other words, conventional calculated LDL substantially underestimates the undesirable effects of fructose. The divergence between calculated LDL and small LDL is especially dramatic. (By the way, this same divergence applies to the studies suggesting that calculated LDL cholesterol is reduced by low fat diets--While calculated LDL may indeed be reduced, small LDL goes way up, a striking divergence.)

This is yet another reason to not rely on this "fictitious" LDL cholesterol value that, inaccuracies notwithstanding, serves as the foundation for a $27 billion per year industry.

"I dream about bread"

25. February 2010 William Davis (14)
Marion sat in my office, sobbing.

It had been 4 weeks since the last piece of bread, bagel, or bun had passed her lips.

"I can't do it! I just can't do it! I've tried to eliminate wheat, but it's making me crazy. I'm having dreams about bread!"

Yes, Timmy, such dark corners of human behavior are truly unveiled by removing wheat from the diet. (See the previous Heart Scan Blog post, Wheat withdrawal.)

This is a real phenomenon: Wheat is the crack cocaine of the masses. Maybe you don't exchange $100 bills in dark corners of an inner city crack house, but I'll bet you paid $3.99 for your latest fix of French bread.

Just in the last 2 weeks, people in my office who have eliminated wheat have experienced:

14 lbs weight loss in 14 days

Increased mental clarity, reduced moodiness, deeper sleep

70% reductions in small LDL

More than 300 mg/dl reductions in triglycerides

Relief from chronic scalp rash


I could go on.

All the while, the USDA, the American Heart Association, the American Diabetes Association, the American Dietetic Association, the Surgeon General's Office all advise you to eat more "healthy whole grains."

70% of people (NOT 100%, but the majority) will experience unexpected health benefits by eliminating this corrupt, unphysiologic product called wheat from their diet.

You won't know until you try.

Prototypical Lipoprotein(a)

25. February 2010 William Davis (23)
Here's the prototypical male with lipoprotein(a):



Several features stand out in the majority of men with lipoprotein(a), Lp(a):

Slender--Sometimes absurdly so: BMIs of 21-23 are not uncommon. These are the people who claim they can't gain weight.

Intelligent--Above average to way above average intelligence is the rule.

Gravitate to technical work--Plenty of engineers, scientists, accountants, and other people who work with numbers and/or technical details are more likely to have Lp(a).

Enjoy high levels of aerobic performance--I tell my Lp(a) patients that, if they want to see a bunch of other people with Lp(a), go to a marathon or triathlon. They'll see plenty of people with the pattern among the aerobically-elite.

Are rabid fans of Star Trek.


Okay, I made the last one up. But the rest are uncannilly true, shared by the majority (though not all) men with Lp(a).

Why? I can only speculate that the gene(s) for Lp(a) are closely linked to gene(s) for intelligence of a quantitative kind and some factor that enhances aerobic performance or yields a desirable emotional state with exercise.

Oddly, the same patterns tend not to occur in women in Lp(a). I have yet to discern a personality or body configuration phenotype among the ladies.

Gastric emptying: When slower is better

20. February 2010 William Davis (18)
When it comes to the Internet and Nascar, speed is good: The faster the better.

But when it comes to gastric emptying (the rate at which food passes from the stomach and into the duodenum and small intestine), slower can be better.

Slower transit time for foods passing through the stomach leads to lower blood sugar, lower blood glucose area under-the-curve (AUC), i.e., reduced blood glucose levels over time. Lower postprandial (after-eating) blood sugars can reduce cardiovascular risk. It can lead to a reduction in net calorie intake and weight loss.

Strategies that can slow gastric emptying include:

--Minimizing fluids during a meal--Drinking a lot of fluids, e.g., water, accelerates gastric emptying by approximately 20%.

--Cinnamon--While the full reason to explain Cassia cinnamon's blood glucose-reducing effect has not been completely worked out, part of the effect is likely to due slowed gastric emptying. Thus, a 1/4-2 teaspoons of cinnamon per day can reduce postprandial blood sugar peaks by 10-25 mg/dl.

--Vinegar--Two teaspoons of vinegar in its various forms slows gastric emptying. The effect is likely due to acetic acid, the compound shared by apple cider vinegar, white vinegar, red wine vinegar, Balsamic vinegar, and other varieties.

--Increased fat content--Fat is digested more slowly and slows gastric emptying time, compared to the rapid transit of carbohydrates.

Not everybody should slow gastric emptying. Diabetics with a condition called diabetic gastroparesis should not use these methods, as they can further slow the abnormal gastric emptying that develops as part of their disease, making a bad situation worse.

However, in the rest of us with normal gastric emptying time, a delay in gastric emptying can reduce blood sugar and induce satiety, effects that can work in your favor in reducing cardiovascular risk.

Genetic vs. lifestyle small LDL

19. February 2010 William Davis (59)
Let me explain what I mean by "genetic small LDL." I think it helps to illustrate with two common examples.

Ollie is 50 years old, 5 ft 10 inches tall, and weighs 253 lbs. BMI = 36.4 (obese). Starting lipoproteins (NMR):

LDL particle number 2310 nmol/L
Small LDL: 1893 nmol/L (1893/2310 = 81.9% of total, a severe small LDL pattern)


Stan is 50 years old, also, 5 ft 10 inches tall, and weighs 148 lbs. BMI = 21.3. Starting lipoproteins:

LDL particle number 1424 nmol/L
Small LDL 1288 nmol/L (1288/1424 = 90.4% of total, also severe)


Both Ollie and Stan go on the New Track Your Plaque diet and eliminate wheat, cornstarch, and sugars, while increasing oils, meats and fish, unlimited raw nuts, and vegetables. They add fish oil and vitamin D and achieve perfect levels of both. Six months later, Ollie has lost 55 lbs, Stan has lost 4 lbs. A second round of lipoproteins:

Ollie:

LDL particle number 1810 nmol/L
Small LDL: 193 nmol/L (193/1810 = 10.6% of total)


Stan:

LDL particle number 1113 nmol/L
Small LDL 729 nmool/L (729/1113 = 65.4% of total)


Ollie has reduced, nearly eliminated, small LDL through elimination of wheat, cornstarch, and sugars, along with weight loss, fish oil, and vitamin D.

Stan, beginning at a much more favorable weight, reduced both total and small LDL with the same efforts, but retains a substantial proportion (65.4%) of small LDL.

Stan's pattern is what I call "genetic small LDL." Of course, this is a presumptive designation, since we've not identified the specific gene(s) that allow this (e.g., gene for variants of cholesteryl ester transfer protein, hepatic lipase, lipoprotein lipase, and others). But it is such a sharp distinction that I am convinced that people like Stan have this persistent pattern as a genetically-determined trait.

Carbohydrate sins of the past

17. February 2010 William Davis (15)
Fifty years ago, diabetes was a relatively uncommon disease. Today, the latest estimates are that 50% of Americans are now diabetic or pre-diabetic.

There are some obvious explanations: excess weight, inactivity, the proliferation of fructose in our diets. It is also my firm belief that the diets advocated by official agencies, like the USDA, the American Heart Association, the American Dietetic Association, and the American Diabetes Association, have also contributed with their advice to eat more “healthy whole grains.”

When I was a kid, I ate Lucky Charms® or Cocoa Puffs® for breakfast, carried Hoho’s® and Scooter Pies® in my lunchbox, along with a peanut butter sandwich on white bread. We ate TV dinners, biscuits, instant mashed potatoes for dinner. Back then, it was a matter of novelty, convenience, and, yes, taste.

What did we do to our pancreases eating such insulin-stimulating foods through childhood, teenage years, and into early adulthood? Did our eating habits as children and young adults create diabetes many years later? Could sugary breakfast cereals, snacks, and candy in virtually unlimited quantities have impaired our pancreas’ ability to produce insulin, leading to pre-diabetes and diabetes many years later?

A phenomenon called glucose toxicity underlies the development of diabetes and pre-diabetes. Glucose toxicity refers to the damaging effect that high blood sugars (glucose) have on the delicate beta cells of the pancreas, the cells that produce insulin. This damage isirreversible: once it occurs, it cannot be undone, and the beta cells stop producing insulin and die. The destructive effect of high glucose levels on pancreatic beta cells likely occurs through oxidative damage, with injury from toxic oxidative compounds like superoxide anion and peroxide. The pancreas is uniquely ill-equipped to resist oxidative injury, lacking little more than rudimentary anti-oxidative protection mechanisms.

Glucose toxicity that occurs over many years eventually leaves you with a pancreas that retains only 50% or less of its original insulin producing capacity. That’s when diabetes develops, when impaired pancreatic insulin production can no longer keep up with the demands put on it.

(Interesting but unanswered question: If oxidative injury leads to beta cell dysfunction and destruction, can antioxidants prevent such injury? Studies in cell preparations and animals suggest that anti-oxidative agents, such as astaxanthin and acetylcysteine, may block beta cell oxidative injury. However, no human studies have yet been performed. This may prove to be a fascinating area for future.)

Now that 50% of American have diabetes or pre-diabetes, how much should we blame on eating habits when we were younger? I would wager that eating habits of youth play a large part in determining potential for diabetes or pre-diabetes as an adult.

The lesson: Don’t allow children to repeat our mistakes. Letting them indulge in a lifestyle of soft drinks, candy, pretzels, and other processed junk carbohydrates has the potential to cause diabetes 20 or 30 years later, shortening their life by 10 years. Kids are not impervious to the effects of high sugar, including the cumulative damaging effects of glucose toxicity.

Saturated fat and large LDL

16. February 2010 William Davis (44)
Here's a half-truth I often encounter in low-carb discussions:

Saturated fat increases large LDL particles


For those of you unfamiliar with the argument, I advocate a low-carbohydrate approach, specifically elimination of all wheat, cornstarch, and sugars, to reduce expression of the small LDL pattern (not to mention reduction of triglycerides, relief from acid reflux and irritable bowel, weight loss, various rashes, diabetes, etc). Small LDL particles have become the most common cause for heart disease in the U.S., exploding on the scene ever since agencies like the USDA and American Heart Association have been advising the public to increase consumption of "healthy whole grains."

This has led some to make the pronouncement that saturated fat increases large LDL, thereby representing a benign effect.

Is this true?

It is true, but only partly. Let me explain.

There are two general categories of factors causing small LDL particles: lifestyle (overweight, excess carbohydrates) and genetics (e.g., variants of the gene coding for cholesteryl-ester transfer protein, or CETP).

If small LDL is purely driven by excess carbohydrates, then adding saturated fat will reduce small LDL and increase large LDL.

If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles.

So to say that saturated fat increases large LDL is an oversimplification, one that can have dire consequences in the wrong situation.

Is glycemic index irrelevant?

14. February 2010 William Davis (20)


University of Toronto nutrition scientist, Dr. David Jenkins, was the first to quantify the phenomenon of "glycemic index," describing how much blood sugar increased over 90 minutes compared to glucose. The graph is from their 1981 study, The glycemic index of foods: a physiologic basis for carbohydrate exchange. The research originated with an effort to characterize carbohydrates for diabetics to gain better control over blood sugar.

Since Dr. Jenkins’ original work, thousands of clinical studies have been performed by others exploring this concept. The food industry has also devoted plenty of effort exploiting it (e.g., low-glycemic index noodles, low-glycemic index cereals, etc.).

Most Americans are now familiar with the concept of glycemic index. You likely know that table sugar has a high glycemic index (60), increasing blood sugar to a similar degree as white bread (glycemic index 71). Oatmeal (slow-cooked) has a lower glycemic index (48), since it increases blood sugar less than white bread.

A number of studies have shown that when low glycemic index foods replace high glycemic index foods (e.g., whole wheat bread in place of cupcakes), people are healthier: less diabetes, less heart attack, less high blood pressure. Books have been written about glycemic index, touting its benefits for health and weight control. Health-conscious people will try to substitute low-glycemic index foods for high-glycemic index foods.

So what’s not to like here?

There are several fundamental flaws with the notion that low-glycemic index foods are good for you:

1) Check your blood sugar after a low-glycemic index food like oatmeal. Most non-diabetic adults will show blood sugars in the 140 to 200 mg/dl range. The more central (visceral) fat you have, the higher the value will be. In other words, an apparently “healthy” whole grain food like oatmeal can generate extravagantly high blood sugars. Repeated high blood sugars of 125 mg/dl or greater after eating increase heart disease risk by 50%.

2) Foods like whole wheat pasta have a low glycemic index because the blood sugar effect over the usual 90 minutes is increased to a lesser degree. The problem is that it remains increased for an extended period of up to several hours. In other words, the blood sugar-increasing effect of pasta, even whole grain, is long and sustained.

3) Low-glycemic index foods trigger other abnormalities, such as small LDL particles, triglycerides, and c-reactive protein (a measure of inflammation). While they are not as bad as high-glycemic index foods, they are still quite potent triggers.

Low-glycemic index foods trigger the very same responses as high-glycemic index foods—they’re just less bad. But less bad does not equate to good. Low-glycemic index foods cause weight gain, trigger appetite, increase blood pressure, and lead to the patterns that cause heart disease.

High-glycemic index foods are bad for you. This includes foods made with white flour (bagels, white bread, pretzels). Low-glycemic foods (whole grain bread, whole wheat crackers, whole wheat pasta) are less bad for you—but they are not necessarily good.

Don’t be falsely reassured by foods because they are billed as “low-glycemic index.” View low-glycemic index foods as indulgences, something you might have once in a while, since a slice of whole grain bread is really not that different from a icing-covered cupcake.