Are there any alternatives to niacin?

In the Track Your Plaque program, we tend to rely a great deal on niacin. When used properly, 90-95% of people will do just fine and achieve their lipid and lipoprotein goals with the help of niacin, along with their other efforts.

Unfortunately, around 5% of people simply can't take niacin without intolerable "hot flush" effects, or occasionally excessive skin sensitivity--itching, burning, etc.

Why does this happen? These 5% tend to be "rapid metabolizers" of niacin, i.e. they convert niacin (nicotinic acid, or vitamin B3) into a metabolite called nicotinuric acid. Nicotinuric acid is the compound responsible for the skin flush. Most people can slow or reduce the effects of nicotinuric acid by:

--Taking niacin with dinner, so that food slow tablet dissolution.

--Taking with plenty of water. Two 8-12 oz glasses usually eliminates the flush entirely in most people.

--Taking with an uncoated 325 mg tablet of aspirin in the first few weeks or months. Eventually, you will need to revert back to a better stomach tolerated dose of 81 mg, preferably enteric coated. But a full 325 mg uncoated can really help in the beginning, or when you have any niacin dose increases, e.g., 500 mg to 1000 mg.

But even with these very effective strategies, some people still struggle. That's when the question arises: Are there any alternatives to niacin?

Well, it depends on why niacin is being used. If you and your doctor are using niacin for:

Raising HDL--Then weight loss to your ideal weight; reduction of processed carbohydrates, especially wheat products; avoidance of hydrogenated ("trans") fats; a glass or two of red wine per day; dark chocolates (make sure first ingredient is chocolate or cocoa, not sugar), 40 gm per day; fish oil; exercise; other prescription agents (fibrates like Tricor; TZD agents for diabetes; cilostazol (Pletal)). Niacin is by far the most effective agent of all, but, if you're intolerant, raising HDL is still possible through a multi-faceted effort.

Reduction of small LDL--The list of effective strategies is the same as for raising HDL, but add raw almonds (1/4-1/2 cup per day), oat bran and other beta-glucan rich foods like oatmeal. Reduction of processed carbohydrates is especially important to reduce small LDL.

Reduction of Lipoprotein(a)--This is a tricky one. For men, testosterone and DHEA are effective alternatives; for women, estrogen and perhaps DHEA. Hormonal preparations of testosterone and estrogen are stricly prescription; DHEA is OTC. I have not seen the outsized benefits on lipoprotein(a) claimed by Rath et al by using high-dose vitamin C, lysine, and profile, unfortunately. We are clearly in need of better alternatives to treat this difficult and high-risk disorder.

Reduction of triglycerides/VLDL/IDL--I lump these three together since they all respond together. If you're niacin intolerant, maximixing your fish oil can be crucial for reduction of these patterns using doses above the usual starting 4000 mg per day (providing 1200 mg EPA+DHA). Reduction of processed carbohydrates, eimination of processed foods that contain high-fructose corn syrup, and weight loss to ideal weight are also very effective. "Soft" strategies with modest effects include green tea (>6 cups per day) or theaflavin 600-900 mg/day; raw nuts like almonds, walnuts, and pecans; exercise; soy protein.

Reduction of LDL--Lots of alternatives here including oat bran (3 tbsp per day), ground flaxseed (3 tbsp per day), soy protein (25 grams per day), Benecol butter substitute (for stanol esters), soluble fibers like pectin, psyllium, glucomannan; raw nuts like almonds, walnuts, and pecans.

In future, should torcetrapib become available (by prescription), this will add to our available tools for these areas when niacin can't be used. Until now, the alternatives to niacin depend on what you and your doctor are trying to achieve. In the vast majority of cases, HDL, small LDL, triglyceride, etc. goals for heart scan score control can be achieved, even when niacin is not well tolerated.

Is flaxseed oil a substitute for fish oil?


This question comes up so frequently that it's worth going over.

Flaxseed oil is a wonderful oil rich in linolenic acid, which may provide health benefits all by itself. Some authorities have speculated that the substantial reduction in heart attack seen in the Lyon Heart Study, the study that demonstrated the healthy power of the Mediterranean diet, is due to linolenic acid.

Flaxseed oil is also rich in monounsaturates and low in saturates, both desirable qualities. Of course, I'm talking here about flaxseed oil, to be distinguished from flaxseed , which are the intact seeds. The seeds themselves also contain the same oils, but contain other components, specifically lignan, a plant fiber with suspected health benefits like reduction in cancer risk.

Despite all flaxseed oil's wonderful properties, it is definitely not a substitute for fish oil. Why do we use fish oil for our coronary plaque control program (trying to reduce your heart scan score)? Several reasons. Fish oil:

--Dramatically reduces triglycerides, usually by 50% or more.
--Dramatically reduces specific lipoprotein classes like VLDL
--Dramatatically reduces, often eliminates, abnormal postprandial (after-eating) lipoprotein patterns, like IDL (intermediate-density lipoprotein)
--Has been conclusively shown to reduce risk of heart attack and death from heart attack (GISSI Prevenzione Trial).
--Has been shwon to reduce risk of stroke.
--Modifies blood clotting parameters, particularly a 20% reduction in fibrinogen.

Flaxseed oil, or linolenic acid concentrate for that matter, do not accomplish any of these effects, all crucial if you are to gain control over your coronary plaque.

Flaxseed oil and flaxseed remain wonderful nutritional agents for their own reasons. But they will not substitute for fish oil in your program. Only fish oil--the real thing--does the job.

If you have coronary artery disease . . . do you know why?

This conversation is aimed primarily at non-followers of the Track Your Plaque program, because if you were a follower, you’d already know the answer!

I saw a woman in the hospital today. She’d just survived her second heart attack one week earlier. At 51 years old, she was understandably shaken, perhaps terrified. She felt that her future was uncertain and, in fact, had discussed with her husband what he should do to prepare for a future without her.

One week earlier, she’d received three stents that successfully aborted her heart attack. But, as is always the case, the modest delays of ambulance transport, the emergency room preliminaries, then of mobilizing an available cardiologist and catheterization laboratory team, totaled nearly two hours before her stent procedure. Inevitably, a moderate amount of damage had been done to her heart.

Her first “event” had been very similar: very little warning, then 911 and the flurry of activity. Both times, the cardiologists (two different physicians) complimented the patient on her prompt action. Both also called her heart attacks “close calls”.

She defied the odds with two near-death events. So, when I met her a week after her last heart attack, I asked an obvious question: “Has anyone told you why you’re having these heart attacks?”

She looked completely puzzled at first. She then said, “No, not really. I just assumed it was genetic. My mother went through the same thing when she was my age. But she didn’t get as far as I have, since they didn’t have these procedures back then.”

To me, this seems inexcusable: This woman had experienced two brushes with death and no doctor had established a cause. Could this woman’s belief be true, that it’s just genetic?

While there are, indeed, genetic causes for heart disease, the vast majority of these genetic causes are 1) identifiable, and 2) correctable. Genetic does not necessarily mean hopeless. It just means that the usual equation of heart disease risk management (heart disease = LDL cholesterol = need for Lipitor) has limited value. It would be like giving penicillin to people for any and all infections. It will work occasionally, but it will fail miserably in a great many cases. Treating LDL cholesterol with statin drugs is just like that.

Perhaps this woman has lipoprotein(a), a serious genetic trait that predicts heart disease at a young age and is largely unaffected by statin drugs. Or, she may have a severe excess of small LDL, only partially suppressed by statins. If she has the combined pattern of lipoprotein(a) and small LDL, that means she has two statin-unresponsive and significant genetic traits. But they respond to niacin, specific nutritional strategies, and several other agents.

The message: If you have coronary disease, you need to insist on knowing why. “It’s genetic” is not an acceptable answer. “There’s no proof of any heart disease causes beyond cholesterol” is also nonsense. “Everyone gets heart disease, or “hardening of the arteries”, eventually. You just got it a little before everyone else” is also patently ridiculous.

Identifying the causes of your coronary disease (or coronary plaque if you’ve had a CT heart scan) is the first step in developing a program of treatment that provides you with control over this disease.

Have you tried inulin yet?

If you haven't yet tried it to facilitate weight loss, it's really worth giving the new inulin-containing product, Fiber Choice "Weight Management", a try.

Recall (from a prior Heart Scan Blog) that inulin is a vegetable-based fiber found in celery, green peppers, etc. that, when exposed to water, expands to many times original volume. This simple phenomenon yields satiety--a feeling of fullness.


The manufacturer of the product has also added green tea, which has been shown in two small clinical studies to enhance weight loss, though by a different route.

We've been advising patients to chew two of the strawberry flavored tablets one hour before every meal (or with breakfast if you eat immediately in the morning). You'll be satisfied with less food and you'll experience less intense food cravings.

Though no one so far has achieved a huge drop in weight, it does seem to enhance a slow, gradual weight loss larger than achieved by diet and exercise alone. And it's very safe and inexpensive. If you give it a try to help you lose weight, let us know what kind of results you've obtained.

Fish oil update on Life Extension

An article of mine came out in Life Extension Magazine and is available on the online version at:

http://www.lef.org/magazine/mag2006/sep2006_report_omega1_01.htm

This is an update on the heart health applications of fish oil.

Or, go to to www.lef.org and put fish oil into your on-site search and you'll come back to it in future.

Of course, it comes with Life Extension's promotion of its supplements.

Although it's not yet available online, the hard copy version of an article I wrote on homocysteine is available in the October, 2006 Life Extension Magazine. If you're not a member of their program, they'll send you a free copy just for signing up for it without obligation. Go to the home page of www.lef.org to do so. Or, Life Extension is available at newstands if you're in a rush or don't want to sign up for a free copy.

More on Vitamin D

If you haven't done so already, you should subscribe to Dr. John Cannell's free newsletter on vitamin D issues. His newest issue is available at:

http://www.vitamindcouncil.com/newsletter/2006-aug.shtml

A sign-up to subscribe is available on the same page.

I continue to be shocked and amazed at the prevalence and magnitude of vitamin D deficiency in the people I see every day. It's been a beautiful summer with very little rain. Most days have been in the 70-80 degree range--very comfortable to be outdoors in the sun and getting skin expoxure to activate vitamin D in the skin.

Yet, in the vast majority of people I see, summer blood levels of vitamin D are virtually indistinguishable from winter levels. Both hover around the 30 ng/ml range. Summer levels in Wisconsin people seem to be no more than 10 ng/ml higher than winter levels. This remains true even in people who spend a lot of their day outdoors gardening, walking, etc. wearing shorts and a short-sleeved shirt, i.e. with plenty of skin surface area exposed.

I'm at a loss to explain precisely why. Yes, it is Wisconsin. But a direct sun overhead, 75 degree day should be providing plenty of sun. My suspicious is that a combination of factors are at work: people are not spending as much time outdoors as they claim; they often seek shade; use sunscreen; and they're overweight. (Excess weight decreases vitamin D blood levels dramatically, yet another reason not to get fat!)

Read more about vitamin D by checking out Dr. Cannell's insightful comments on the unfolding vitamin D story. He holds nothing back.

Why not just get "perfect" lipids and call it a day?

What if you achieved the Track Your Plaque lipid targets: LDL cholesterol 60 mg/dl, HDL 60 mg/dl, and triglycerides 60 mg/dl?

After all, these are pretty stringent standards. Compared to national guidelines (the ATP-III Guidelines of the National Cholesterol Educational Panel), the Track Your Plaque 60-60-60 goals are laughably ambitious. There's a lot of wisdom hidden in those numbers. The triglyceride level of 60, for instance, is a level at which triglycerides become essentially unavailable for formation of triglyceride-containing lipoprotein particles such as small LDL and VLDL.

If you get to the 60-60-60 target, isn't that good enough? What if you just held your values there and went about your business? Will coronary plaque stop growing and will your CT heart scan score stop increasing?

Sometimes it will. But, unfortunately, many times it will not. The experience generated through clinical trials bear this out. Studies like the St. Francis Heart Study and the BELLES Trial both showed that just reducing LDL cholesterol is insufficient to stop plaque growth. Beyond the Track Your Plaque experience, there's no clinical trial experience that shows whether the 60-60-60 approach does any better.

In our experience, achieving 60-60-60 is indeed better than just reducing LDL. That makes sense. Just raising HDL from the average of 42 mg/dl for a male, 52 mg/dl for a woman adds advantage. Compound this with triglyceride reduction from the plaque-creating equation, and you've doubled success.

But there's even more. What if you had hidden patterns not revealed by conventional lipids? How about lipoprotein(a)? Small LDL? Postprandial (after-eating) abnormalities? Hypertensive effects (more common than you think)!

In 2006, stopping the increase in your heart scan score is, for most of us, not just a matter of taking Lipitor or its equivalent and sitting back. For nearly all of us, stopping the progression of your score is a multi-faceted effort.

Hospitals: Then and Now

It's 1920. The hospital in your city is a facility run by nuns or the church. It's a place for the very ill, often without hope of meaningful treatment, but nonetheless a place where surgeries take place, babies are born, the injured and chronically ill can find care. No one has health insurance and there's no Medicare. Everyone pays what they can. The hospital is accustomed to doling out plenty of care without compensation. For that reason, they welcome donations and sometimes will build new additions or other facilities in honor of a major donor.

Volunteeers are common, since the wards are understaffed and generally suffering from a shortage of trained nurses and personnel associated with the church. Drugs, such as they are, are often prepared from basic ingredients in the hospital pharmacy. Product representatives hawking medicines and devices are virtually unheard of.

Though their therapeutic tools are limited, the physicians are a proud group, dedicating their careers to healing. The majority of the medical staff volunteer large portions of their time to care for the poor who come to the hospital with very advanced stages of disease: metastatic tumors, advanced heart failure, debilitating strokes, overwhelming septicemia, etc.

Hospitals are usually governed by a board of clergy and physicians who make decisions on how to apply their limited resources and continually seek charitable donations.


Fast forward to present day: Hospitals are high-tech, professional facilities with lots of skilled people, complicated equipment,and capable of complex procedures. While they still house people with advanced illnesses, the floors are also filled with people with much earlier phases of disease. In general, they do a good job, with quality issues scrutinized by a number of official agencies to police practices, incidence of hospital-related infections, medication errors, care protocols, etc.

The hospital of 2006 is a more more effective place than the hospital of 1920. But its aims and operations are different, also. Though some churches are still involved in hospitals, more and more are owned by publicly-traded companies that answer to shareholders--shareholders who want share value to increase. Though donations are still sought, much of the revenues are obtained by concentrating on profitable, large-ticket procedures. More procedures are often generated by advertising.

Because they operate to generate profits, several hospitals in a single city or region compete with one another. The 21st century has therefore witnessed the phenomenon of hospital-owned physicians: more and more practicing physicians are employees of their hospital. That way, the physician brings all his patients and procedures to his hospital, not to a competitor. The top of the funnel is the primary care physician, who tends to see all disease when it first occurs. The primary care physician then sends the patient to the specialist, who is obliged (by contract) to perform his/her procedure in the hsopital paying their salary.




Representatives from companies manufacturing and selling expensive hospital equipment and drugs are everywhere, falling over themselves to gain attention of the physicians using their equipment and the hospital buyers who make purchasing decisions. Millions of dollars can be transacted with just one sale.

The number of volunteers has dwindled. The poor and uninsured are commonly diverted elsewhere, often to a government-funded, and often second-rate, institution. Hospitals measure success by comparing annual revenues and numbers of major procedures.

The hospital of 2006 is a vastly different place than 1920. If you're expecting charitable treatment, compassion, and selfless care, you're in the wrong century. In 2006, the hospital is a business. You don't expect charitable treatment at Wal-Mart or from your car dealer. Don't expect it from your hospital. They are businesses and you are a customer. Recognize this fact, lose the nostalgia for the hospitals of yesterday, and a lot more will become clear to you.

The dreaded small LDL particle

Brian is a 59-year old landscape architect whose starting CT heart scan score was 276.

Brian's food choices at the start were deplorable: a pound of sausage per week, sometimes more; butter on anything and everything; up to two pounds of cheese per week; hot dogs; etc. His lipoproteins were accordingly just as miserable: low HDL, high triglycerides, excessive (postprandial, or after-eating) IDL. Small LDL was a particularly stand-out pattern, with 95% of all LDL particles in the small category.

Brian made a dramatic turnaround in lifestyle and corrected all of his patterns--except for small LDL. After one year, small LDL still occupied 95% of all LDL particles, even though the quantity of LDL had been reduced. In order to help convince Brian that correction of his small LDL was going to be necessary to achieve control oover coronary plaque, I suggested that he undergo another heart scan. His score: 435, or a 57% increase.

Each day that passes, I gain more and more respect for small LDL as a cause for coronary plaque growth. Conventional thought among lipid experts is that small LDL should no longer be a factor if total LDL (e.g., LDL particle number) is reduced. But our experience suggests otherwise: when small LDL persists, we tend to see continued, sometimes frightening, plaque growth.

I therefore asked Brian to intensify his efforts: additional weight loss off his somewhat prominent abdomen (since visceral fat increases small LDL), further reduce wheat products and processed carbohydrates, increase niacin (to 1500 mg per day), and use more raw almonds and oat bran.

Don't let small LDL get the best of you. It is a nasty, sometimes persistent abnormality that has impressive effects on plaque growth.

Winning Through Intimidation

Do you remember the book, Winning Through Intimidation by author Robert J. Ringer?



In his 1984 bestseller, author Ringer details how to succeed in business by overwhelming clients and competition by appearing hugely successful and powerful. Rather than a business card, he'd hand out an elegant book to represent himself. He'd show up in a limousine to a meeting, even when he could barely afford it. He used these tactics, even when he was a small-fry, in commercial real estate and built a successful business following such techniques.

This reminds me a lot of what happens in conventional medical practice: The large and successful hospitals, filled with trained staff and technology, exude legitimacy and success. How can they possibly be wrong? Such overwhelming know-how and multiple levels of expertise mustbe right!

Let's be grateful that we do have access to such high-tech, capable care. Unfortunately, just as Mr. Ringer used deceptive practices to appear something he wasn't, this is also true in hospitals. Not all physicians have your best interests in mind. Their principal concern is how profitable your care can be for them--can you be persuaded to have your stent, bypass, etc.. After all, look around you: Aren't all this equipment and personnel impressive? Aren't you intimidated?

The patient that most recently drove home this issue for me recently was a smart and capable executive who came in for consultation. He had been told by his internist that a surgery (to replace his aorta, a HUGE procedure) was probably necessary. In my view, it was not--his process was simply not that far progressed. The risks for danger over the next several years was virtually nil. Unfortunately, this man, now confused and worried, sought an opinion from the chief of thoracic surgery (in the usual white coat and with professorial demeanor, I'm sure) in a major metropolitan hospital (in Chicago), who promptly rushed him off to the operating room.

The pathology report, cleverly not mentioned in any other of the hospital documentation, showed what I had suspected: this man had mild disease that wasn't even close to requiring surgery. But, with all that technology, $100,000 or so of costs, chief of surgery who looked the part, etc.--they must be right!

Robert Ringer's concepts only ring too true for hospitals and some of the unscrupulous physicians in practice. Don't allow yourself to be intimidated.
One hour blood sugar: Key to carbohydrate control and reversing diabetes

One hour blood sugar: Key to carbohydrate control and reversing diabetes

Diabetics are instructed to monitor blood glucose first thing in the morning and two hours after eating. This helps determine whether blood sugar is controlled with medications like metformin, Januvia, Byetta injections, or insulin.

But that's not how you use blood sugar to use to prevent or reverse diabetes. Two-hour blood sugars are also of no help in deciding whether you have halted glycation, or glucose modification of proteins the process that leads to cataracts, brittle cartilage and arthritis, oxidation of small LDL particles, atherosclerosis, kidney disease, etc.

So the key is to check one-hour after-eating (postprandial) blood sugars, a time when blood glucose peaks after consumption of carbohydrates. (It may peak somewhat sooner or later, depending on factors such as how much fluid was in the meal; protein, fat, and fiber content; presence of foods like vinegar that slow gastric emptying; the form of carbohydrate such as amylopectin A vs. amylopectin B, amylose, fructose, along with other factors. Once in a while, you might consider constructing your own postprandial glucose curve by doing fingersticks every 15 minutes to determine when your peak occurs.)

I reject the insane notion that after-eating blood sugars of less than 200 mg/dl are acceptable, the value accepted widely as the cutoff for health. Blood sugars this high occurring with any regularity ensure cataracts, arthritis, and all the other consequences of cumulative glycation. I therefore aim to keep one-hour after-eating glucoses 100 mg/dl or less. If you start in a pre-diabetic or diabetic range of, say, 120 mg/dl, then I advise people to not allow blood glucose to go any higher. A pre-meal blood glucose of 120 mg/dl would therefore be followed by an after-eating blood glucose of no higher than 120 mg/dl.

No doubt: This is strict. But people who do this:

--Lose weight from visceral fat
--Heighten insulin sensitivity
--Drop blood pressure
--Drop HbA1c and fasting glucose over time
--Reduce small LDL and other carbohydrate-sensitive measures

By the way, if you inadvertently trigger a high blood sugar like I did when I took my kids to the all-you-can-eat Indian buffet, go for a walk, bike, or burn the sugar off with a 30-minute or longer physical effort. Check your blood sugar again and it should be back in desirable range. But then learn from your lesson: Eliminate or reduce portion size of the culprit carbohydrate food.

Comments (27) -

  • Might-o'chonri-AL

    8/2/2011 6:11:40 AM |

    Glyco-sylation occurs inside a cell's endoplasmic reticulum lumen when certain  carbohydrates  (in the form of N-linked oligo-saccharides) meld with a newly folded protein that gets translated into  a glyco-protein.  There are different rates of activation and de-activation  between glyco-sylated and un-glycosylated proteins; this affects how that protein migrates as it tries to perform it's job and how  glycation can induce degenerative states.  Tissue cells with endoplasmic reticulum stress can exasperate certain disease progression because such "stress" there promotes more glycosylation.

  • Annabel

    8/2/2011 12:40:42 PM |

    I couldn't agree more with the advice to test every 15 minutes as a means of discovering your own "sugar curve." When I tried this, I found that my own peak falls pretty consistently at 75 minutes after beginning a meal. Testing at 2 hours completely overlooks my highest blood glucose levels.

    It's a particularly good technique for those folks whose A1c levels are higher than their fingersticks would predict...it's almost surely because they're doing their sticks way past their glucose peak.

    When test strips cost up to a buck apiece, it may feel hard to justify using six or eight of them on a single meal--but what you learn may save tens of thousands in medical bills!

  • Curt

    8/2/2011 1:31:12 PM |

    Another great article - thank you! I'm curious about your thoughts on controlled 1 hour blood sugars (mine are rarely over 110) but baseline levels that aren't much lower. Typically in the 95-105 range. I will get something in the 80s occasionally, but 100 is more common. I never really spike - even a high carb meal will only get me to 130s or so and that never really happens as I don't eat much sugar/starch at all.

    Another quick question: You've mentioned a couple times recently about this way of eating being particularly good for VISCERAL fat. That is exactly what I've found. Tremendous benefits and I feel great. I have leveled out for a while (months) in fat loss, however, with a good amount of subcutaneous fat still present. Is there another protocol for getting after this type of fat? I'm already no wheat, low carb, paleo.

    Thanks again for your excellent articles! Always learning something new.......

  • ShottleBop

    8/2/2011 1:38:20 PM |

    Do you have citations to support your statement that glycation occurs at BGs of 100 or more?  This is one of the more-commonly discussed issues on diabetes discussion boards--but folks are wont to ask for backup.

  • Jeff C

    8/2/2011 1:47:11 PM |

    Regarding glycation specifically...

    1. Do you agree that fructose ("frucation") causes more AGE than glucose?
    2. What to you make of Ray Peat's assertion that poly-fats are much more glycalating than glucose?

    "The so-called "advanced glycation end products," that have been blamed on glucose excess, are mostly derived from the peroxidation of the "essential fatty acids." The name, “glycation,” indicates the addition of sugar groups to proteins, such as occurs in diabetes and old age, but when tested in a controlled experiment, lipid peroxidation of polyunsaturated fatty acids produces the protein damage about 23 times faster than the simple sugars do." (Fu, et al., 1996)." - Ray Peat

  • Richard

    8/2/2011 3:21:55 PM |

    Thanks for the great article!
    I've just begun tracking blood sugars closely, changed my diet to one very low in carbs and no grains, and am determined to find ways to keep at it. I've started a blog just track my progress and keep me honest: http://transformation-transformative.blogspot.com/
    I'll also try the 15 minute testing to see where my personal peak in blood sugar occurs.
    Again, many thanks!

  • steve

    8/2/2011 3:31:08 PM |

    Hi Dr. Davis:  What is the relationship between fasting BG taken at the Dr's office and A!C?  My fasting BG level is 73.5 but my A1C is 5.4.  I would have expected the A1C to more correspond to the fasting measurement; in the case of my wife it does.  Is it related more to the red blood cells lingering around longer or lipoprotein particles which increases the chance of glycation?  Recently had a larger than normal amount of carbs in a meal- rice and blueberries and BG spiked to 119, not to bad, but will experiment with carb portion to keep under 100 as BG may be a contributing factor to my CAD.  I am also a hyperabsorber of fat despite being an ApoE 3/3.

    As an aside, i have sent around a link of one of your interviews regarding Wheat Belly and many eyes have been opened as well as many looking to buy the book.  Might not be a bad idea to have a link to any of your interviews on Wheat Belly posted to this site.
    Thanks for the enlightening good work!

  • Dr. William Davis

    8/3/2011 12:23:09 AM |

    Hi, Shottle--
    This will be the topic of an upcoming discussion. The documentation of this effect is quite extensive. It is no longer a matter of "if" but "how much."

  • Dr. William Davis

    8/3/2011 12:25:11 AM |

    Hi, Jeff--
    This is one of oranges and apples comparisons.
    Fructose does indeed induce flagrant glycation. Glucose induces glycation, though less vigorously.

    However, there is a separate but very poorly named process called exogenous glycation which has less to do with glycation than with oxidation of fats.

    This will be the topic of future discussions.

  • Dr. William Davis

    8/3/2011 12:26:22 AM |

    My first thought is that, if weight loss is ongoing, there is a temporary situation of insulin resistance that generally dissipates with weight stabilization.

    It's also possible that your pancreas has inadequate baseline production of insulin. I'm hoping it's the first possibility.

  • Dr. William Davis

    8/3/2011 12:28:05 AM |

    Hi, Steve-

    You will find that, if you did frequent fingersticks around the clock, the highish A1c reflects the higher blood glucose values that occur after meals.

    Thanks for the feedback on the Wheat Belly project. I will indeed crosslink some of the more relevant discussions.

  • Might-o'chondri-AL

    8/3/2011 2:39:31 AM |

    Advanced glycation end products (AGE) involve some of haemoglobin's hydro-carbon Beta side chain valine residue linking up to non-polar "glucose" aldehyde compounds and certain non-"glucose" aldehydes. Various pathological kinds of AGEs can occur from distinct events; in one situation it is macrophage activity producing enzymatic myelo-peroxidase, which can activate hypochlorite favoring a serine amino acid wing to form up to make the AGE called glyco-aldehyde.

    Probably the AGE called methyl-glyoxal is the one most relevant to diabetes prevention; since Type 1 diabetics blood serum levels of methyl-glyoxal is +/- 6 times higher than normal. This AGE can be formed when the byproduct triose-phosphate (triose = subset of carbs) is generated from the glycolytic pathway called  Embden-Meyerhof; this  byproduct risks being made into methyl-glyoxal.

    Maybe the most well known AGEs are the non-enzymatic Amadori products formed via hydrolysis; one is called glyoxal coming from glucose oxidation. And the other Amadori type AGE is 3-deoxy-glucosone (3DG), which requires fructo-selysine and the fructos-amine 3 kinase cascade to shuffle together 3DG.

  • Might-o'chondri-AL

    8/3/2011 2:40:38 AM |

    Diabetes reveals the problem with AGEs; this is because diabetics risk incurring kidney nephro-pathy, One of the pathological results is oxidative kidney stress, which limits sodium (Na) excretion thereby fostering  hyper-tension . When AGEs like 3DG, glyoxal & methyl-glyoxal  (among others, like pentosidine ) circulate into the kidneys their carbonyl compounds  are hard to clear by the kidneys; the side effect is to engender  uric uremia problems and meanwhile levels of carbonyls build up in what is called "carbonyl stress".
    Japan research of the plant compound chamaemeloside found that in humans it lowered levels of the AGEs 3DG & pentosidne better than any other natural remedy; optimal response was reduction of down to 1/5 th of subject's starting levels.  Chamaemeloside is the active compound in chamomile (Anthemis noblis); the extraction formula was 1 Kg of chamomile flowers steeped covered in 20 Lt. water for 3 hours at 80* celcius ( a lab temperature probably not critical for home remedy preparation).

  • Peter Silverman

    8/3/2011 12:56:13 PM |

    Volek and Phinney in their new book about carbohydrate restriction think that as you increase  fat from 30% to 60% of your diet, insulin resistance increases, then it drops when you go above 60%.  It seems that among the most experienced researchers of carbohydrate restriction, there's little consensus about the optimal amount of fat or carbs.  Ron Krausse, for instance, thinks 35% to 45% is optimal.

  • steve

    8/3/2011 5:23:50 PM |

    Peter:
    When these researchers talk about carb levels are they considering vegetables to be carbs, or just fruits, grains, potatoes?

  • frank weir

    8/3/2011 6:41:32 PM |

    You must mean, "can exacerbate certain disease progression...." meaning: to increase the severity, violence, or bitterness of; aggravate

  • frank weir

    8/3/2011 6:59:22 PM |

    This is wonderful information BUT I wonder if it might be unfortunate if folks who routinely have post-prandials of 120 to 140 take your 100 level as a sign of "failure"...things are seldom so cut and dried, black and white. I don't know if I'm hitting 100 or less  after every meal, but my A1C has dropped from 7.5 to 5.8 since last November restricting carbs. And I've lost 30 pounds. I will begin to be more dogmatic about one-hour glucose checks but my rough sense is that I'm not at 100 or less a majority of the time. But I might be wrong about that. Do you see what I'm getting at? Glucose control is an ongoing process that includes lots of self education since most GP's are not keen AT ALL on restricting carbs, including mine. When I read your post, my initial feeling was, "Cripes, 100 after EVERY meal? Don't think I can do that...."

  • Might-o'chondri-AL

    8/4/2011 1:05:26 AM |

    From another commentator here, in an  earlier thread of Dr. Davis' here is how to use HbA1c to determine your average blood glucose level (note: this is not a morning "fasting" level) .
    1st: multiply your HbA1c by 28.7
    2nd: subtract 46.7 from 1st amount
    3rd: take last number as your average waking hours mg/dL blood glucose over last  few months  
    ex:  HbA1c of 5.4 x 28.7 = 159.98 minus 46.7 = 108.28 mg/dL of average blood glucose level

  • Peter Silverman

    8/4/2011 2:24:31 AM |

    They don't count non-starchy vegetable as carbs.

  • ShottleBop

    8/4/2011 3:15:11 AM |

    Thanks for the heads up!

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  • Stephanie

    8/4/2011 2:13:27 PM |

    Dr. Davis,
    I have found that if I take my carb level too low (below 50g per day) that my fasting blood glucose levels actually go up rather than down.  If my carb intake is closer to 70-80, my fasting glucose is lower.

    Have you had this experience with some of your patients?  Can you shed any light onto what might be happening?

    Thanks!
    Stephanie

  • Anne

    8/4/2011 2:34:11 PM |

    Non-starchy vegetables do have carbs and I do have to count them. A half cup of broccoli can have about 6 carbs and since I limit my carbs to no more than 15g/meal, that broccoli on my plate is significant.

    I found getting a scale that reads carbs too was an important tool for me. I found I was ofter overestimating how much of a low carb veggie I could eat. If my blood sugar starts to rise, I go back to measuring and that seems to get me back on track.

    Anne

  • majkinetor

    8/14/2011 1:25:56 PM |

    I think thats normal, its commonly encountered on paleo forums/blogs. It has something to do with physiological insulin resistance, Petro @ Hyperlipid talked about. Look here:

    http://high-fat-nutrition.blogspot.com/2007/10/physiological-insulin-resistance.html

  • majkinetor

    8/14/2011 1:38:24 PM |

    I wouldn't suggest that everybody blindly follow CHO < 50g / day. As always, its about the context. People usually forget that. We mostly extrapolate from results of people who already have metabolic problems.

    Anyway, I am currently perfectly healthy apart from some minor dermatology problems (eczema).
    When I have prolonged periods of reduced CHO input (around 50g / day), I eventually start having some mucus problems. Dry eyes particularly, but also joint pain. I am not 100% sure if its about low carb diet, but it looks like it. Now I target 75g < CHO < 100g per day by adding small potato and a bit more chocolate to my diet.

    I think overemphasizing carb reduction is not good thing for most people. Carbs should go down by pretty big amount for most people, but not to extreme. In anyway, its better to measure then to guess. My sugar is never above 110 after meal and fasting is always around 95.

  • John F

    8/13/2012 9:48:10 AM |

    I decided to take this advice and have been tracking my 60 mins postprandial blood glucose for the past two days to see if all the years I've been low carbing have been making any difference. Especially working my way through different foods to see how they affect me and I've ranged from 64 mg/dl to 97 mg/dl so I'm pretty hapy.

    However this evening 60 minutes after my dinner of panfried steak with a creamy cajun sauce I got a reading of just 55 mg/dl. A lot of websites say this is too low. I'm 32, healthy male, 5,9", weigh 160 lbs, not diabetic and I don't feel sick so I'm not sure what to make of this low reading. The only thing I did was finish a hard CrossFit workout about 30 mins before I had dinner... so a total of 90 minutes before the blood glucose test.

    Any advice on what this "low" reading means? I'm hoping it's normal and means I'm burning fat!

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