Can I stop my Coumadin?

Here I go again.

While I will try to keep this blog on topic, i.e., coronary heart disease prevention and reversal using nutritional and other natural strategies, I believe that a "critical mass" of frequently asked, though off topic, questions keep cropping up.

One such question revolves around Coumadin, or warfarin.

Somehow, my Nattokinase scam blog post draws traffic about Coumadin. I tried to make the point that a conventional blood thinning agent like Coumadin that undoubtedly has undesirable side-effects cannot be replaced by an agent that has an uncertain track record. In the case of nattokinase, no track record.

To illustrate how far wrong the "nattokinase as replacement for Coumadin" idea can go, here is a question from Anna:


I came across your blog while perusing.

I am a bit bummed because I have been on Coumadin (warfarin) for around 22 years since I was 6 years old. I have a mechanical heart valve (St. Jude's), as I have heart-related issues, including hypertrophic obstructive cardiomyopathy.

Well, it is just that the warfarin seems to interact with nearly everything. I feel like I can not get the nutrients my body requires. I desire to consume more raw foods and vegan foods, though I do not want anything to damage my heart valve or risk a stroke/heart attack or internal bleeding.

I have been underweight the majority of my life, malnourished , currently am still somewhat underweight, though enjoying food again, as I had what mimicked Crohn's Disease for several years (horrendous pain), from which I am in remission now. I was diagnosed with osteoporosis, which may or may not be caused from consuming warfarin.

Is it possible to get off of warfarin and effectively keep my blood thinned ? I currently take 1.5 mg to 2 mg dosage. Does the warfarin destroy Vitamin K and if so does that mean while on warfarin I never get the Vitamin K nutrients even if I did consume foods with it in it?

Thank you
Anna


No, sorry, Anna. Stopping Coumadin with your unique issues, i.e., a prosthetic mechanical heart valve (likely mitral, judging by your history of hypertrophic obstructive cardiomyopathy, in which the patterns of blood flow ejected from the heart disrupt the natural mitral valve function) and cardiomyopathy, can be fatal. Without blood thinning, the mechanical heart valve can trigger blood clot formation, since it is a foreign object implanted into the bloodstream.

There are no natural alternatives available with track records confident enough to bet your life on. Aspirin nor Plavix are blood thinners, but platelet inhibitors. These two agents, while they work for other forms of arterial (but not venous) blood clot inhibition, will not work for your unique situation.

Likewise, a purported oral lytic agent like nattokinase should not be substituted for Coumadin. Even if there was plausible science behind it, you should demand substantial evidence that it provides at least blood thinning equivalent to Coumadin. Should a blood clot, even a small one, form in or around the prosthetic valve, the valve can stop working within seconds. This can lead to death within minutes.

I believe it would be foolhardy to bet your life based on the marketing--let me repeat: MARKETING--of a "nutritional supplement" by supplement manufacturers eager to make a buck.

Nor are there any other nutritional supplements that can safely replace the Coumadin. I wish that were NOT true, as I am no stranger to the long-term dangers of Coumadin and I am a big believer, in general, in nutritional supplements. I am a BIGGER believer, however, in the truth. Weighing the options available to us today, there really is no rational choice but to remain on Coumadin.

By the way, I tell my patients to eat a substantial amount of green vegetables while they take Coumadin. I know that conventional advice is to reduce or eliminate green vegetables due to their content of Coumadin-antagonizing vitamin K. I think this is wrong, also. Green vegetables are the best foods on earth. They reduce risk for cancer, diabetes, bone disease, and coronary heart disease.

To obtain the benefits of green vegetables without mucking up your blood thinning (your "protime" or International Normalized Ratio, INR), I advise my patients who take Coumadin to eat green vegetables--but do so every day in relatively consistent quantities, so that the protime or INR is not disrupted and remains reasonably constant. It may mean that your total dose of Coumadin may be somewhat higher, e.g., 3 or 4 mg instead of 2 mg, but the dose is immaterial outside of blood thinning. That way, you obtain all the wonderful health benefits of green vegetables while maintaining fairly consistent blood thinning/protime/INR. Coumadin does not block all the health benefits of vegetables, only those related to vitamins K1 and K2.

With regards to protecting yourself from the osteoporosis promoting effects of Coumadin, I would be sure to follow a program of natural bone health, such as the one I discussed in Homegrown osteoporosis prevention and reversal. You will have to be extra careful, however, with the vitamin K2. Ideally, you have a doctor knowledgeable about vitamin K2 who can assist you in managing K2 intake while on Coumadin. This is something you can definitely NOT manage on your own. (I am a big believer in self-managed care, but this is way beyond the limit.)

Lastly, it is my belief that anyone with an inflammatory bowel condition, such as Crohn's disease or ulcerative colitis, should absolutely, positively, and meticulously AVOID WHEAT and all other gluten sources (such as rye, barley, and oats). Even if you test negative for celiac markers (e.g., anti-gliadin antibodies, emdomysium and transglutaminase antibodies), the enhanced intestinal permeability will allow wheat proteins, such as gluten, to gain ready entry into the bloodstream. Not to mention that wheat should have no place in the human diet anyway, in my view.

Homegrown osteoporosis prevention and reversal

I don't like to stray too far off course from discussions of heart disease and related issues in this blog. But the question of bone health comes up so often that I thought I'd discuss the strategies available to everybody to stop, even reverse, osteoporosis.

Coronary atherosclerotic plaque and bone health are intimately interwoven. People who have coronary plaque usually have osteoporosis; people who have osteoporosis usually have coronary plaque. (The association is strongest in females.) The worse the osteoporosis, the greater the quantity of coronary plaque, and vice versa. The two seemingly unconnected conditions share common causes and thereby respond to similar treatments.

Incredibly, rarely will your doctor tell you about these strategies. Your doctor orders a bone density test, the value shows osteopenia or osteoporosis, and a drug like Fosamax or Boniva is prescribed. As many people are learning, drugs like this can be associated with severe side-effects, such as jaw necrosis (death of the jaw bone), a dangerous and disfiguring condition that leads to loss of teeth and disfigurement, followed by reconstructive surgery of the jaw and face. These are not trivial effects.

Note that drugs are approved by the FDA based on assessment of efficacy and safety, NOT proven equivalence or superiority to natural treatments.

In order of importance (greatest to least), here are strategies that I believe are important to regain or maintain bone health. Indeed, I have seen many women increase bone density using these strategies . . . without drugs of any sort.

1) Vitamin D restoration--Vitamin D is the most important control factor over bone calcium metabolism, as well as parathyroid function. As readers of this blog already know, gelcap forms of vitamin D work best, aiming for a 25-hydroxy vitamin level of 60-70 ng/ml. This usually requires 6000 units per day, though there is great individual variation in need.

2) Vitamin K2--If you lived in Japan, you would be prescribed vitamin K2. While it's odd that K2 is a "drug" in Japan, it means that it enjoys the validation required for approval through their FDA-equivalent. Prescription K2 (as MK-4 or menatetranone) at doses of 15,000-45,000 mcg per day (15-45 mg), improves bone architecture, even when administered by itself. However, K2 works best when part of a broader program of bone health. I advise 1000 mcg per day, preferably a mixture of the short-acting MK-4 and long-acting MK-7. (Emerging data measuring bone resorption markers suggest that lower doses may work nearly as well as the high-dose prescription.)

3) Magnesium--I generally advise supplementation with the well-absorbed forms, magnesium glycinate (400 mg twice per day) or magnesium malate (1200 mg twice per day). Because they are well-absorbed, they are least likely to lead to diarrhea (as magnesium oxide commonly does).

4) Alkaline potassium salts--Potassium as the bicarbonate or the citrate, i.e., alkalinizing forms, are wonderfully effective for preservation or reversal of bone density. Because potassium in large doses is potentially fatal, over-the-counter supplements contain only 99 mg potassium per capsule. I have patients take two capsules twice per day, provided kidney function is normal and there is no history of high potassium.

5) An alkalinizing diet--Animal products are acidic, vegetables and fruits are alkaline. Put them together and you should obtain a slightly net alkaline body pH that preserves bone health. Throw grains like wheat, carbonated soft drinks, or other acids into the mix and you shift the pH balance towards net acid. This powerfully erodes bone. Therefore, avoid grains and never consume carbonated soft drinks. (Readers of this blog know that "healthy, whole grains" should be included in the list of Scams of the Century, along with Bernie Madoff and mortgage-backed securities.)

6) Strength training--Bone density follows muscle mass. Restoring youthful muscle mass with strength training can increase bone density over time. The time and energy needs are modest, e.g., 20 minutes twice per week.

Note that calcium may or may not be on the list. If on the list at all, it is dead last. When vitamin D has been restored, intestinal absorption of calcium is as much as quadrupled. The era of force-feeding high-doses of calcium are long-gone. In fact, calcium supplementation in the age of vitamin D can lead to abnormal high calcium blood levels and increased heart attack risk.

These are benign and easily incorporated strategies. They are also inexpensive. I challenge any drug to match or exceed the benefits of this combination of strategies. Keep in mind that strategies like vitamin D restoration provide an extensive panel of health benefits that range far beyond bone health, an effect definitely NOT shared by prescription drugs.

Your enlarged aorta

The thoracic aorta lives happily within the chest.

The aorta is the main artery of the body that emerges from the heart, located just under the sternum. It is the "tree trunk" from which all the major arteries branch off to the rest of the body: the arms, brain, abdominal organs, pelvis, and legs. The aorta receives the high-pressure blood ejected directly out of the heart muscle.

However, there are evil forces in the body that work to weaken the aorta. When the aorta is weakened, it enlarges. Enlarged aortas also tend to grow atherosclerotic plaque. Plaque in the aorta poses long-term risk for stroke and and mini-strokes ("transient ischemic attacks," or TIAs), due to fragmentation.

There are many enlarged aortas in this world. I see at least several every week. It is fairly common, particularly in people with high blood pressure and cholesterol abnormalities, as well as those who are overweight. Smokers get it really bad.

Conventional thinking is that, once an aorta enlarges, it will inevitably continue to enlarge at the average rate of 2.0 mm per year (resulting in 1.0 cm enlargement over 5 years). For this reason, conventional discussions on the topic of thoracic aortic aneurysms all say something like "Enlarged aortas should be monitored yearly. Surgical replacement should proceed when the aorta reaches a diameter of 5.5 cm."

This is because an aortic diameter of 5.5 cm is associated with much greater likelihood that the aorta will rupture (fatal within minutes) or the internal lining will tear, a "dissection." The surgery is a major undertaking that involves opening the chest and usually replacing the aortic valve and inserting a synthetic aorta. The procedure is high-risk, especially if any branch arteries are involved.

So putting a stop to any further aortic enlargement is a worthwhile goal. Unfortunately, conventional thought is that there is nothing you can do to stop the inevitable growth of the thoracic aorta.

Nonsense. There are a number of efforts you can make to halt further increase in aortic diameter. (My experience in this is anecdotal and unpublished, but now numbers several hundred patients.)

There are two categories of factors that cause the aorta to increase in diameter:

1) Internal pressure--Think of blood pressure as the internal inflating pressure on this "balloon." Keeping the "inflating pressure," i.e., blood pressure, low exerts substantial effect on slowing growth of aortic diameter. I aim for normal BP or lowish BP (less than 130/80, preferably 100/70).

2) Factors that weaken the aortic wall--Processes like inflammation, glycation, lipoprotein deposition, and nutritional deficiencies will serve to weaken the supportive tissue of the aorta. For that reason, correction of lipoprotein abnormalities (e.g., small LDL and lipoprotein(a)), reductions in carbohydrate intake and thereby blood glucose/glycation, and "normalization" of vitamin D, vitamin C supplementation (for collagen crosslinking), and omega-3 fatty acids all play a role.

To push even farther, there may be additional advantage to following strategies that impair the production and activity of a crucial enzyme that lives within the aortic wall: matrix metalloproteinase, or MMP. MMP degrades the collagen and other supportive tissues within the aorta, weakening it and permitting expansion. Blocking MMP may prove to be among the most powerful new strategies to halt aortic expansion.

Compounds that have potential MMP-inhibiting effects include:
--Vitamin D--A substantial effect
--Resveratrol--One of the polyphenols from red wine
--Doxycycline--This old antibiotic often used for acne treatment has, in preliminary studies, shown important MMP-blocking effects and slowed aortic expansion.

Anyway, there you have it. A bit complicated, but a "recipe" that has failed me only rarely.

Extreme carbohydrate intolerance

Here's an interesting example of what you might call "extreme carbohydrate intolerance."

May is a 44-year woman who has now had her 7th stent placed in her coronary arteries. She lives on a diet dominated by breads, breakfast cereals, muffins, rice, corn products, along with some real foods.

Her conventional lipid panel and other lab values:

Total cholesterol 346 mg/dl
Triglycerides: 877 mg/dl
HDL cholesterol: 22 mg/dl
LDL cholesterol: incalculable
(Recall that LDL cholesterol is usually a calculated, not a measured value. The excessively high triglycerides make the standard calculation invalid--more invalid than usual.)

Fasting blood glucose: 210 mg/dl
HbA1c (a reflection of previous 60-90 days average glucose): 7.2% (desirable 4.5% or less)
ALT (a "liver enzyme"): 438 (about five-fold normal)


At 5 ft even and 138 lbs (BMI 27.0), May appears small. But the modest excess weight is all concentrated in her abdomen, i.e., in visceral fat.

By lipoprotein analysis via NMR (Liposcience), May's LDL particle number was 2912 nmol/L, or what I would call a "true" LDL of 291 mg/dl. (Drop the last digit.) Of the 2912 nmol/L LDL particles, 2678 nmol/L, or 92%, were small.

The bad news: This pattern of extremely high triglycerides, extremely high LDL particle number, low HDL, predominant small LDL, and diabetes poses high-risk for heart disease--no surprise. It earned her 7 stents so far. (Unfortunately, she has made no effort whatsoever to correct these patterns, despite repeated advice to do so.)

The good news: This collection is wonderfully responsive to diet. LDL particle number, small LDL, triglycerides, blood glucose, and HbA1c drop dramatically, while HDL increases. Heart disease will at least slow, if not stop.

It's amazing how far off human metabolism can go while indulging in carbohydrates, particularly a genetically carbohydrate-intolerance person. (Actually, I wouldn't be surprised if May's diet, as bad as it seems to you and me, still fits within the dictates of the USDA food pyramid.) The crucial step in diet to correct this smorgasbord of disaster is elimination of carbohydrates, especially that from wheat, cornstarch, and sugars.

What's for breakfast? Egg bake

Heart Scan Blog reader and dietitian, Lisa Grudzielanek, provided this recipe in response to the post, What's for breakfast?

Lisa, by the way, is one of the rare dietitians who understands that organizations like the American Dietetic Association have made themselves irrelevant. She therefore advocates diet principles that work, not just echoing the idiocy that emanates from such organizations, often driven by economics more than science. Lisa works in the Milwaukee area and has proven a useful resource person for my patients who have required extra coaching in the Track Your Plaque diet principles.

Egg Bake
My favorite breakfast is what I call an "egg bake." Others may refer to it as a "quiche."

Take a variety of fresh vegetables. This time of year is great for farmers' markets.

I typically use fresh chopped organic spinach, bell peppers, red & white onions, scallions, broccoli, mushrooms, cherry tomatoes halved and, if desired, meat (nitrite-free ham or leftover chicken breasts).

1) Chop veggies and place in casserole dish.
2) Add meat and handful of cheese of your choice.
3) Scramble 8 eggs & little bit of milk & pepper.
4) Add to casserole dish and mix/coat veggies with egg mixture.
5) Put in oven at 450 degress for 30 minutes.

Yummy, ready to eat breakfast that is so easy for the work week.

What's for breakfast?

If you eliminate wheat from breakfast and otherwise adhere to a low-carbohydrate dietary approach, what is there to eat for breakfast?

If you take out English muffins, bagels, all breakfast cereals, pancakes, waffles, and toast, what's left to eat?

Actually, there's plenty left to eat. It just may not look like the traditional American notion of "breakfast." (The traditional idea of breakfast was is, in part, due to the legacy of Dr. John Harvey Kellogg, who, in the latter part of the 19th century, ran a sanitarium in Battle Creek Michigan. He and his brother, Will Keith Kellogg, discovered the idea of turning grains into flakes, the birth of the breakfast cereal. Subscribe to the idea of breakfast cereal for breakfast and you subscribe to the ideas of a man who would administer four enemas for you today to cure your cancer or rheumatism.)

Here are a few ideas. By no means is this meant to be a comprehensive list, just a starting point for a few new breakfast food ideas.

--Eggs--Of course, eat the yolk. Eat three yolks. Scrambled, "fried," (not really deep-fried, of course), hard-boiled, poached, as an omelette. Add pesto, olive oil, vegetables, mushrooms, salsa.

--Ground flaxseed--As a hot cereal with your choice of water, milk (not my favorite because of insulin effects; the fat is immaterial), full-fat soy milk (yeah, yeah, I know), unsweetened almond milk. Add walnuts, blueberries, etc. Ground flaxseed is the only grain I know of that contains no digestible carbohydrates.

--Lunch and dinner--Yes, if you cannot have breakfast foods for breakfast, then have lunch and dinner, meaning incorporating foods you ordinarily regard as lunch and dinner foods into your day's first meal. This means salads, leftover chicken from last night, soup, raw vegetables dipped in hummus or guacamole, stir fry, etc.

--Cheese--For something quick, grab a chunk of gouda or emmentaler along with a handful of raw almonds, walnuts, or pecans. Because of the excess acidity of cheese (along with meats, among the most acidifying of foods), I usually try to include something like a raw pepper or avocado, foods that are net alkaline.

--Avocados--Cut in half, scoop out contents. They're quick and delicious, when available.

I hesitate to mention it, but I sometimes will have tofu, cubed and flavored with whatever is available--soy sauce, miso, pickled vegetables. My mother was Japanese, so I'm comfortable with this, though many people are not.

Anyway, that's a partial list that nonetheless can get you started on a wheat-free, low-carb breakfast.

If you are just starting out, you will notice a number of fundamental changes. You may first experience the characteristic "withdrawal" effect: mental fog and fatigue that lasts about a week. Energy then picks up, often substantially. This is followed by gradually reduced appetite: You will be far less hungry. You will require less food, less often, since appetite will be driven by physiologic need, not the appetite-stimulating properties of wheat (and cornstarch, high-fructose cornsyrup and sucrose).

By the way, do not skip breakfast unless it's part of an occasional fasting effort. Skip breakfast, wind down metabolism, get fat. I am impressed at how consistent skipping breakfast backfires in those who think that it helps you control weight.

I also welcome any suggestions on what you eat as part of your wheat-free, low-carb breakfast. (Thanks for the great suggestions on the last blog post, Anna.)

Wheat hip

You've heard of wheat belly. How about wheat hip?

Recall that the innocent appearing wheat belly is actually a hotbed of inflammatory activity beneath the surface. The visceral fat of the wheat belly, i.e., fat kidneys, fat liver, fat intestines, fat pancreas, produces abnormal inflammatory signals, such as various interleukins, tumor necrosis factor, and leptin. These are the inflammatory signals that create insulin resistance and diabetes, heart disease, hypertension, and cancer.

These same inflammatory mediators are able to enter the joint spaces, such as those in your hips, knees, and hands. This leads to osteoarthritis, the exceptionally common form of arthritis that affects 1 in 7 Americans. In particular, the level of leptin in joints mirrors that in blood, a phenomenon that has been associated with joint destruction.

The previously widely-held notion that arthritis is simply a wear-and-tear phenomenon due to the mechanical stress of excess weight is proving to be an oversimplification. Arthritis is also part of the carbohydrate-driven, weight-increasing, inflammatory condition of insulin resistance or metabolic syndrome.

Throw into this cytokine storm the fact that glycation, i.e., glucose modification of proteins, also causes cartilage destruction. The cells of human cartilage lack the ability to divide, so the cartilage cells you had at age 18 are the cartilage cells that you will hopefully still have at age 80. However, high blood sugars (glucose) glycate the proteins in cartilage. (Wheat raises blood glucose higher than almost all other foods, higher than a Milky Way bar, higher than a Snickers bar.) The process is irreversible and cumulative. Because cartilage has next to no capacity for repair or regeneration, it becomes brittle. Over years, it essentially crumbles, leading to the "bone on bone" that prompts conversations about total hip and total knee replacement.

So that ciabatta or blueberry muffin in your mouth takes you a step or two closer to joint destruction via heightened inflammation arising from the visceral fat of the wheat belly, worsened by glycation of high blood sugars after carbohydrate consumption.

My solution: Lose the ciabatta.

Men's lingerie is on the second floor

Consume wheat products, like poppyseed muffins, raisin bagels, and whole grain bread, and you trigger the 90- to 120-minute glucose-insulin cycle.

Blood glucose goes way up (more than almost any other known food), triggering insulin release from the pancreas. Glucose enters cells as a result, blood glucose plummets. You get hungry, shaky, and crabby, reach for another wheat or other sugar-generating food to start the roller coaster ride all over again.

Repetitive insulin triggering grows this thing I call a "wheat belly," the protuberant, hang-over-the-belt fat you see everywhere nowadays. Wheat belly fat is really visceral fat. Visceral fat means you have fat kidneys, fat intestines, fat pancreas, and fat liver, all causing the belly to protrude in the familiar way we've all come to recognize.

Visceral fat is special fat. Unlike the fat in the backside, thighs, or arms, visceral fat triggers inflammatory responses that are evident in such measures as tumor necrosis factor, interleukins, and leptin, as well as drops in the protective hormone, adiponectin.

Visceral fat also, oddly, triggers estrogen release. Estrogen triggers growth of breast tissue. That's why females with wheat bellies have up to four-fold (400%) greater likelihood of breast cancer.

Men also experience excess estrogen from the visceral fat wheat belly, causing "man boobs." This B-cup phenomenon means that inflammation is raging beneath the surface, all due to this thing you're wearing around your waist.

I wasn't aware until recently that male breast reduction surgery is a booming business growing at double-digit rates. So are special clothes to help men conceal their expansive breasts.

Perhaps the USDA is in cahoots with Playtex.

10,000 units of vitamin D

Joanne started with a 25-hydroxy vitamin D level of 23 ng/ml--severe deficiency.

What made this starting value even worse was that it was drawn in August after a moderately sunny summer spent outdoors. (Last summer, not this summer.) It therefore represented her high for the year, since vitamin D levels trend lower as fall and winter set in. This suggests that her winter level was likely in the teens or even single digits. In addition, note that, at age 43, Joanne has lost much of her ability to activate vitamin D in the skin.

So I advised that she take 6000 units of an oil-based gelcap per day, a dose likely to generate the desired blood level, which I believe is 60-70 ng/ml.

Four months later, her 25-hydroxy vitamin D level: 39.9 ng/ml--still too low. So I advised her to increase her dose to 10,000 units per day. Several months later, her 25-hydroxy vitamin D level: 63.8 ng/ml--perfect.

However, on hearing that she was taking 10,000 units vitamin D per day, Joanne's primary care physician was shocked: "What? Stop that immediately! You're taking a toxic dose!" So Joanne called me to find out if this was true.

No, of course it's not true. It's not the dose that's toxic, but the blood level it generates. Although it varies, vitamin D toxicity, as evidenced by increased blood calcium levels, generally does not even begin to get underway until at least 120-130 ng/ml, perhaps higher. Rarely, a dose of 2000 units per day will generate a level this high. In others, it may require 24,000 or more units per day to generate such a high level.

So it's not the dose that's toxic, but the blood level of 25-hydroxy vitamin D it generates.

Provided you and/or your doctor are monitoring 25-hydroxy vitamin D blood levels, the dose is immaterial. It's the blood level you're interested in.
Blood glucose 160

Blood glucose 160

What happens when blood glucose hits 160 mg/dl?

A blood glucose at this level is typical after, say, a bowl of slow-cooked oatmeal with no added sugar, a small serving of Cheerios, or even an apple in the ultra carb-sensitive. Normal blood sugar with an empty stomach, i.e., fasting; high blood sugars after eating.

Conventional wisdom is that a blood sugar of 160 mg/dl is okay, since your friendly primary care doctor says that any postprandial glucose of 200 mg/dl or less is fine because you don't "need" medication.

But what sort of phenomena occur when blood sugars are in this range? Here's a list:

--Glycation (i.e., glucose modification of proteins) of various tissues, including the lens of your eyes (cataracts), kidney tissue leading to kidney disease, skin leading to wrinkles, cartilage leading to stiffness, degeneration, and arthritis.
--Glycation of LDL particles. Glycated LDL particles are more prone to oxidation.
--VLDL and triglyceride production by the liver, i.e., de novo lipogenesis.
--Small LDL particle formation--The increased VLDL/triglyceride production leads to the CETP-mediated reaction that creates small LDL particles which are, in turn, more glycation- and oxidation-prone.
--Glucotoxicity--i.e., a direct toxic effect of high blood glucose. This is especially an issue for the vulnerable beta cells of the pancreas that produce insulin. Repeated glucotoxic poundings by high glucose levels lead to fewer functional beta cells.

A blood glucose of 160 mg/dl is definitely not okay. While it is not an immediate threat to your health, repeated exposures will lead you down the same path that diabetics tread with all of its health problems.

Comments (28) -

  • Pater_Fortunatos

    2/25/2011 8:20:12 PM |

    There are lot of unusual and interesting formulations you are using, but I really can't understand the meaning of this one:

    "Glycation and of LDL particles."

    Maybe my english is not the best (I am no native english speaker).Maybe you could enlighten me?

    About the article. Now I realize that during 35 years of life, I had lots of such glycemic  values and not having any idea about effects.
    Do you have any ideea about glycemic index if I eat quite a lot of fruits? (can't control it lately).

    Thank you!

  • Might-o'chondri-AL

    2/25/2011 8:50:30 PM |

    Hi Pater_F.,
    I just read this post too, so see your quote shows a word to edit out. Remove the word "and", then it reads correctly "Glycation of LDL ...."

  • Flavia

    2/25/2011 9:05:59 PM |

    Hi Dr. Davis,

    What do you think is a safe amount of carbs to eat in one sitting? No more than 50 maybe? What really gets me is the aging!! I do not want wrinkles!

    For a 5'4, 125lb woman, what would you recommend is the top limit of carbs to have per meal to avoid this?

  • susan

    2/25/2011 10:54:14 PM |

    Thanks for the info about how the body handles high glucose levels. Funny you should mention a glucose of 160…

    I generally stay with the low carb lifestyle. I’ve been checking my glucose on a fairly regular basis and it generally runs in the high 80s to high 90s. Exercise can bring it down to mid 70s. Fasting levels are creeping up into the low 100s.

    Late yesterday afternoon, however -- after a good low carb day -- I succumbed to my baser urges and consumed several handfuls of mini Reese’s PB cups. Pretty dumb, I know.  

    2 hours later, BG = 161  -- whoa, I guess that was even dumber than I thought
    After a good low carb dinner, BG = 99  -- respectable, considering  
    This morning’s AM Fasting BG = 150 – what the heck??  (it’s been running a little high, but not that high
    Large coffee w/ cream on the way to work, BG = 118  -- getting there, slowly  
    Low carb breakfast and lunch, BG = 113  -- wow! Never dreamed it would take this long  

    Well, I knew it was a stupid thing to do. Now I know how stupid it really was. I’m sure my BG will continue to come back down to a reasonable level. I’ve been toying with the idea of rejoining the gym and starting the Slow Burn program. Guess it’s time.

  • Dr. William Davis

    2/26/2011 12:41:00 AM |

    Thanks for catching the typo, Pater and Might.

    HI, Flavia--

    It is truly an individual thing. For some, it's 20, 30, or 50 grams. For others, it's zero.

    Body size, age, genetics, recent exercise, et. all enter into the equation. This is why I am a fan of checking postprandial blood glucoses.


    Hi, Susan--

    It can really be a sobering experience. When this happens to me, I feel awful for several hours, sometimes all day. I've learned that it's not worth the momentary indulgence.

  • belly fat exercises

    2/26/2011 7:22:01 AM |

    Yes insulin lowers blood sugar levels by converting glucose to glycogen which is stored in the liver and by increasing cell permeability to glucose.

  • Might-o'chondri-AL

    2/26/2011 8:41:02 AM |

    Individual liver condition may influence how dangerous the blood sugar reaction actually is.

    "Fasting, overnight, trigs (triglycerides) are mostly bound to VLDL. But once eat there are trigs complexed to chylomicrons (from the intestine), IDL (intermediate density  lipo-protein, a VLDL spin off), in standard VLDL and even HDL.

    HDL, "good" lipo-protein, is the returner of cholesterol from the peripheral regions of the body back to the liver; it too carries trigs. In the liver hepatic trig lipase enzymes hydrolize (cleave) off the HDL's trig load; and those trigs can then get complexed to both IDL and chylomicrons.

    The re-circulated trigs add to the new trigs certain foods generate. When we look specificly at LDL bound trigs those trigs were passed on over from VLDL trigs, whether if were freshly tagged onto VLDL or from overnight fasting VLDL trigs.

    In the case of chylomicron trigs and IDL trigs the lipase enzymes in the adipose (fat) tissue and
    intestine, as well as triglyceride lipase enzymes in the liver, cleave those trigs into component free fatty acids and glycerol. In practical terms that's when we get fat in a form we can "get fat" from.

    Fat in the liver tissue also causes extra fatty acids to go out into the blood stream and, among other tissue, into skeletal muscles. The muscles of course do have the potential to use fat as fuel.

    Only problem is when insulin resistance starts to develop progressively in the liver, when fat in there messes with our trig balancing act. The back log concentration of intra-hepatic trigs is one of the conditions
    when post meal hyper-insulinism is dangerous.

    Then there is a further complication. When insulin resistance starts to go on outside the liver those peripheral tissues keep performing lypolysis. They are
    trying to burn fat while waiting on blood glucose stuck outside their cells. So even more freed up fatty acids go back in the blood to burden the liver.

    At this stage the liver
    can't re-esterfy (break back down) the burden of free fatty acids into trigs. So more gets built into fat inside the liver and eventually can lead to blockages (steatosis). It is a vicious cycle looping trigs and free fatty acids in a double "whammy" on the liver.

    To recap the immediately preceeding. A new/young/healthy liver takes in a meal, produces some extra trigs and sends it out tagged to VLDL. Once liver damaged/old/fat there are high levels of free fatty acids in circulation, the liver response to insulin drops (liver insulin resistance), the liver passes along meals glucose but the skeletal muscles are full of trig derivatives (di-acyl-glycerides, to be precise), so the muscles don't pick up the glucose either.

    Once an individual's liver fat is interfering with things to an even worse degree there are further complications. Namely the trigs complexed to VLDL get out of the liver less and it is mostly chylomicron trig and IDL trig complexes circulating in the blood.

    In fact, a measurement where total trigs keeps dropping can
    indicate chronic liver disease. And in hepatitis the physical synthesis of VLDL is
    progressively reduced; the virus inhibits protein movement in the liver microsome needed for VLDL production.

    Remember there is a liver triglyceride lipase enzyme. It has several functions and can act as a binder for many other lipoproteins, including LDL.

    Individuals who geneticly, or due to pathology (like in hepatitis), produce too little of this enzyme have another problem. This enzyme insufficiency makes the blood
    level of HDL complexed trigs keep rising (trig can't be cleaved off HDL who brought it back to liver)so HDL can't do it's "good" cholesterol job.

    The same enzyme insufficiency also lets trigs complexed to LDL, IDL and chylomircrons become elevated in the blood stream.

  • Might-o'chondri-AL

    2/26/2011 9:04:46 AM |

    Cut off my post's theory, too long.

    If individual has no fat in the liver (or minimal liver fat that is not enough to mess up trig metabolism), then blood sugar spike generated trigs not a problem. This can be genetic propensity, liver circadian rhythm co-incidence &/or life style.

    Those laying down liver fat, geneticly impinged &/or life style disadvantaged seem to be getting good advice from Doc.

  • Anne

    2/26/2011 1:14:56 PM |

    Watch out if you are in intensive care. The American College of Physicians now recommends that blood sugar be maintained between 140-200mg/dL. Their main concern is blood sugar going too low. In Hospital Blood Sugar Levels Should be Higher

    They will also feed you an ADA approved high carbohydrate diet to guarantee those highs.

  • Nigel Kinbrum

    2/26/2011 3:05:29 PM |

    @Dr. Davis: Are those your own BG readings after eating oatmeal? If low-carb/keto adapted, eating a pile of carbs is a bad idea as glycolytic pathways are down-regulated.

    @Anne: How about wearing a bracelet with important medical information on it in the event of becoming unconscious?

  • Anonymous

    2/26/2011 3:09:43 PM |

    These recent blog entries regarding blood sugar are extremely simple even to the point of being vague.

    I have found a site that goes into great detail regarding blood sugar, its control, and the problems associated with both high and low blood sugar levels. The blogs entries are so successful that they were edited and published as a book.

    The author continues to blog weekly and includes practical detail, as well as references to current medical science. Don't let the label "diabetes" throw you. There is a tremendous amount of information regarding how to avoid T2DM with improved blood sugar control. How and when to check your blood sugar, using your meter to determine the impact of what you eat on blood sugar, the deleterious effects of higher than normal blood sugars, even what is normal sugar are all addressed and in useful detail...there are even discussions regarding low carb and paleolithic diets. If you want 5-10 quickly and poorly written sentences on a topic, read the HeartScan blog. If you are interested in reading entire well written intelligent essays visit these sites below. I think that the "MD" label misleads many readers. Don't let the fact that the writer of the Blood Sugar 101 sites is not an "MD" throw you. She is a diabetic and has lived with it for several years. Her approach to medical treatment is that it should be "evidence-based" which seems often missing from other sites.

    Take a few minutes to review,

    Blood sugar 101 (general information site)
    http://www.phlaunt.com/diabetes/

    Associated blog site
    http://diabetesupdate.blogspot.com/

  • Anonymous

    2/26/2011 4:59:13 PM |

    What happened to the post about the Blood Sugar site? It seems to have been deleted. I am sute that I saw it here earlier. Does anyone know the url for the site. it looked interesting.

  • Anonymous

    2/26/2011 6:45:18 PM |

    yeah i saw it too. seems poster was a bit critical of Dr. Davis last several postings. sorry don't have the web sites mentioned. didn't know that you could delete a post that you don't like.

  • Anonymous

    2/27/2011 2:30:17 AM |

    @ Anne,

    In the ICU, there is risk with both too high and too low a blood sugar.  Perhaps 140-200 is an unhappy medium where risks are balanced.

    'Recent research, including a study in the Feb. 15 issue of the Annals of Internal Medicine, has found that the use of intensive insulin therapy comes with an increased risk of low blood sugar (hypoglycemia) which can be deadly. The study also concluded that using intensive insulin therapy to significantly lower blood sugar levels isn't associated with greater improvements in health outcomes.'

    Many ICU patients aren't eating anything anyway.  It isn't until after they are on the general medical floor that the ADA diet is given, and their sugars chased down to a lower range with insulin and/or drugs!

    Teresa

  • Might-o'chondri-AL

    2/27/2011 2:32:27 AM |

    11,000 Koreans studied by Stamford's Sun Kim, M.D. published in Journal Clinical Endocrinology (2011):

    27% had fatty liver (ultrasound diagnosis); 47% of those with fatty liver had high fasting insulin vs. only 17% of those without fatty liver having high fasting insulin. All subjects with fatty liver also had high blood sugar, high trigs and low HDL.

    Participants followed for 5 years; and data correlated on those with, and those without fatty liver who became clinically diabetic. Study conclusion is that fatty liver in participants preceeds Type 2 Diabetes by +/- 5 years in a statistically significant number (ie: no fatty liver = less risk of developing adult onset diabetes).

    Doc undoubtably has new patients and blog readers who have mildly fatty livers that don't think he's right. He should make them hire Revelo to put them through their paces instead.(Joke attempt there Revelo, not a personal digg.)

  • Anonymous

    2/27/2011 5:07:52 PM |

    I am familiar with the web sites that were mentioned in the deleted post. I did not think the post was very critical at all. It only said that these sites provided more detailed information regarding the recent blood-sugar related topics being discussed here. By the way, these sites contain a good deal information that you will only see around here at the Doctor’s pay-to-join blog.

  • revelo

    2/27/2011 7:59:44 PM |

    The martinet in me would be happy to whip anyone into shape who needs it. Seriously though, even the most extreme exercise program is child's play compared to what happens when you get sick. Imagine someone saying to you: "First I'm going to saw through your ribcage, and then I'm going to slice through your arteries..." It's like something out of a horror movie. And yet that is what happens during open heart surgery. And then there are those ailments for which there is no medical relief, surgical or otherwise. Be afraid of getting sick, be very afraid. Be willing to endure any sort of diet and exercise regime to avoid getting sick.

  • Dr. William Davis

    2/27/2011 8:08:44 PM |

    Ni, Nigel--

    No, not my personal blood sugars, but typical responses I've seen in many patients.


    Re: deleted comments
    I have no problem with criticisms. I do have problems with people saying things like "you're an asshole" or similar comments that add nothing to the conversation.

    I now have a zero-tolerance policy for rudeness, but NOT criticism.

  • Anne

    2/27/2011 9:16:04 PM |

    @ Nigel - I like MediAlert bracelets.

    @ Teresa - IMHO, the ADA meal plan is much too high in carbohydrates. It does not make sense to me to cause an elevated blood sugar and then use a medication to bring it down. How about lower the carbohydrate load and use minimal medication? You can find this program in Dr. Richard K Bernstein's book "Diabetes Solution".

    I am T2 and am able to keep my blood sugars in a good range by diet alone by greatly limiting my carbohydrates.  

    I understand those in the ICU present with many challenges to obtaining optimal blood sugar control.

  • Anonymous

    2/28/2011 1:50:55 AM |

    @ Anne,

    I was concerned that anyone without medical training who didn't look at the article linked to in your post wouldn't realize that there are risks to both too low and too high blood sugars in the intensive care unit.

    The comment about the ADA diet and using insulin and drugs to control blood sugars, was meant to poke fun at the ADA.  I apologize.  

    Teresa

  • Helen

    2/28/2011 11:54:36 PM |

    I don't doubt that high blood sugars are harmful, but I do wonder if when they are very transient if the effect is so terrible.  I have always had poor glycemic control.  In terms of going to 200 on a glucose tolerance test, I have diabetes.  But my blood sugars have been lower on a low-fat diet than they were on a low-carb one.  It also now takes me three times as many carbs to get to 175 or so than when I was on a low-carb diet and they are disposed of very quickly - I get down to 75-90 within an hour and a half.  I do think I have a MODY-like form of diabetes - that I'm not particularly insulin resistant.  I'm still not sure what all is going on, but I've been checking my blood sugar rather compulsively for 10 months, and this is what I've found.  

    I'm nearly 45 years old, have great blood pressure, triglycerides of 44 (this may be part of my particular MODY diabetes profile - a few types have genetically low triglycerides), high HDL and low LDL.  I look young for my age.  I don't have any microvascular complications.  I'm still very concerned about my glucose levels, but whatever diet I'm on my BG goes up above 160 with nearly every meal (I can catch it if I test at just the right time), but transiently.  A high-carb diet makes my fasting glucose and between-meal readings much lower, so the overall average is lower.

    Perhaps M-Al is right, if you are  storing fat in your liver, or if you are insulin resistant, it's a different story.  Perhaps anti-oxidant status, overall diet quality, and other lifestyle factors have an impact that large-scale studies don't pick up, since the numbers and outcomes of those with a Dunkin Donuts diet are averaged in with those with a whole foods diet, one along the lines of what Stephan Guyenet suggests.  

    I do think I'm not normal, and a "normal" person with the blood sugars Dr. Davis cites is courting trouble.  But I'm worried about getting too obsessive about my normal, since there's only so much I can do to control it.  It might be that I can be healthy even given the givens.  

    I also think it's worth considering that someone on a low-carb diet often is going to have more trouble disposing of a sudden influx of carbs.  It takes about three days of consistently higher carbs before the body adjusts.  Some people clearly develop higher triglyerides and other trouble on a high-carb diet.  My point is just that the context of one's particular phenotype is important - and sometimes tough to figure out.

  • Might-o'chondri-AL

    3/1/2011 5:56:01 AM |

    Hi Helen,
    I don't want to over step blog protocol, so this is just feedback. The blood test for glycated hemoglobin shows how the blood glucose dynamic is playing out the last couple of months.

    HbA1c is that test and, I believe, Doc set a result over 5.5% is undesireable. Maybe it would give you some insight to how your ranges of blood sugar are playing out.

    Someone here (thank you sir) recommended summitcountymedicalsociety.prepaidlab.com ; I recently used them. Credit card payment gets you an email prescription (to print out) for blood tests, they've cooperating independent
    blood drawing clinics nationwide and lab results are emailed to you. (I needed their 800 phone # help some and they resolved every issue promptly.)

    Charge = US$13 for HbA1c test plus +/- $16 for processing fee(one fee for unlimited tests, it seemed). Their prices were so much cheaper than other online options.

  • Helen

    3/1/2011 11:51:40 AM |

    Thanks, M-Al -

    At initial Dx, my A1C was 6.4.  After seven months on a strict low-carb diet (like 60 g carbs/day) and a 20 lb weight loss (I'd only been 10 lbs overweight at Dx, for the first time in my life, but I lost 20 during that time.  I've now lost nearly 30, not all for good reasons.) it was down to 6.0.  I'm monitored quarterly and am due for another A1c.  We'll see if my lower readings are borne out by the test.  I don't expect miracles, but I'm doing the best I can.  Some people's blood sugars only come down so much.  Metformin was ineffective for me and insulin would probably be dangerous, since my BG dips so far on its own post-prandially after peaking.

  • Anonymous

    4/16/2011 9:58:46 AM |

    DISCLAIMER, MY ENGLISH IS NOT VERY GOOD and this is loong SO BARE WITH ME ON THIS,I HAVE READ @ printed all this BLOG AND DROVE MY FAMILY(DOCTORS) and FRIENDS @  CARZY 1 ! THANKS!

    So i finally got my  glucometer:  OneTouch Ultra (ahh) + brand new strips (ouch) not cheap here where i live...  my old man  (doctor, lives on a diet of coffee, diet soda, bread pasta, cookies, candy etc, etc, etc + a few drugs... and is tall and "lean") thinks im completely crazy. ( im 33, 78kgr, also lean and muscular)

    so my pattern: OMP-day  fasting
    ( 23h, 24h, 27h, 30 hrs regular fasts) + 3 day wrkts
    (home, chin ups, push ups, squats) rest of the tm im mostly sedentary

    my readings so far...

    D1: 13-4

    10:00 >  71mg/dL >  FS@BS (prior that  day ate a bit of candies... pascuas)

    11:00 >  ERROR (didnt put the right code, got pissed @ didn't test)

    D2: 14-4  (no carb)

    3:07 > 70mg/dL >  FS@BS

    EAT: meat (+)yolks(+) cheese (+) butter (-) water

    4:05  > 81 mg/dL > AE@BS

    5:05  > 77 mg/dL > AE@BS

    D3 15-4 "workout" day (chin ups)  + carb
    ERROR, 2 little blood, !"·$%didn't test  (assumed 70mg/dL  FS@BS)



    11:00 >EAT: (pWRKOUT)

    meat(-) yolks (+) cheese(-) butter (-) tomato juice (+) 350CC Whole MILK+ 100G " 60% CHOCOLATE"  ( 37g carbs. aprox 20@30g sucrose + milk sugars )
    this baby

    http://www.chocolatesaguila.com.ar/uploads/info_nutricional/tabletas_rellenas_3344.pdf

    ( copy paste if u care)

    11:00 >EAT

    12:05 >  75 mg/dL > AE@BS

    12:20 > 72 mg/dL  > AE@BS

    1:06 >  82 mg/dL > AE@BS  
    ( waited 2 long there?)

    2:09  > 70 mg/dL > AE@BS

    6:12 > 67 mg/dL > AE@BS

    D3 16-4  
    ("rest day" upped the carbs anyway)

    "FS@BS"  (didn't bother to test. low as usual, i guess)

    1:00 > ??? mg/dL
    EAT: salted peanuts... roasted in vegetable oil... 100gr (could not find my chocolate...)

    2:00 > ??? mg/dL
    EAT:
    one lean, small cut of meat+ ham+ 6 yolks omelet fried in butter,  the usual 100g cheeses- Roquefort, sardo, pategras,cuartirolo,feta, 6tbs tomato juice, salt, peeper, (napolitanta)

    Dessert: -2-  ice cold glasses of 300CC WHOLE MILK + 2 TBS of Cheap sugary cocoa powder  (approx 20@30g sucrose total + milk sugars)

    3:05 > 107 mg/dL (!)

    - moved my arse a bit and did 2  slow sets of dumbbell squats, (40 reps with16k w total, super slow and easy)

    3:36 > 83 mg/dL

    4:37 > 66 mg/dL

    ok, any comments ? are my number ok?  what makes more sense , eating chocolate ( fiber, slower absrs possible less sucrose, or drinking  milk?  (talking desert here) i do not  eat vegetables, ( just, pepers, tomato juice and mushrooms) do not  eat fruit, and of course do not even touch gluten nor refined crap, and always try to limit my PUFA, and fructose load.

    also im thinking i should test my BS levels differently?  maybe  eating one (large) H fat, H 2 moderate protein, meal per day changes things a bit?  so maybe waiting 1 hrs is not enough ( thats why i used milk x 2 today, and did not wrkout to speed things a bit)

  • Anonymous

    4/16/2011 10:19:41 AM |

    edit, im 68 kgr ( not 78) ... always do the same mistake, maybe i need to gain weight!

  • Anonymous

    4/16/2011 11:01:28 AM |

    OneTouch Ultra Meter
    Eating pattern: OMP-day  
    ( 23h, 24h, 27h, 30 hrs  fasts)


    D1 REST DAY

    3:07 > 70mg/dL >  FS@BS

    EAT: meat (+)  yolks (+) cheese (+) butter ( -)  water

    4:05  > 81 mg/dL > AE@BS

    5:05  > 77 mg/dL > AE@BS


    D2 WRK DAY

    11:00 >  71mg/dL  FS@BS

    EAT: meat (-) yolks (+) cheese(-) butter (-) tomato juice (+)  +  350CC Wf MILK + 100G " 60% dark chocolate"

    12:05 >  75 mg/dL > AE@BS

    12:20 > 72 mg/dL  > AE@BS

    1:06 >  82 mg/dL > AE@BS

    2:09  > 70 mg/dL > AE@BS

    6:12 > 67 mg/dL > AE@BS


    D3  REST DAY (upped the carbs, + added liquid sugar, wrst  case)


    1:00 > ??? mg/dL
    EAT: salted peanuts... roasted in vegetable oil... 100gr

    2:00 > ??? mg/dL
    EAT:one lean, small cut of meat+ ham+ 6 yolks omelet fried in butter, 140g cheese, 6tbs tomato juice,  (napolitanta) 2  ice cold glasses of 300CC W MILK WITH 2 TBS of Cheap sugary cocoa powder  (aprox 20@30g sucrose + milk sugars)

    3:05 > 107 mg/dL (!)

    -did 2   slow sets of dumbbell squats, (40 reps with16k w total, no effort)

    3:36 > 83 mg/dL

    4:37 >  66 mg/dL

    Hypoglycemia?
    any opinions about my numbers, (imm33) should i ditch the milk @dark chocolate and eat "healthy vegetables" and "fruit" (no)


    should i wait longer 2 test my BS? (slower digestion time, one meal and all)

  • Anonymous

    4/17/2011 8:50:49 AM |

    today


    17-4 > WRKT

    9:00 > 69 mg/dL

    10:58 > EAT (6 YOLKS, CHEESE, BUTTER, 1TBS TOMATO JUICE - OMELET + 400GR MINCED MEAT, 6 STRIPS BACON, 5TBS TOMATO JUICE, BUTTER)

    2:07 > END

    DISHWASHING

    2:16 > 350cc WHOLE MILK

    2:21 > 100G 60% chocolate

    2:34 > END

    2:40 > 300cc WHOLE MILK + 1 TBS SUGAR (nesquik)

    3:01 > 71mg/dL

    3:36 > 74mg/dL

    4:39 > 83mg/dL

    5:42 > 74mg/dL

    650cc milk + lots of  sucrose... where is the zomg 160 blood glucose doctor? (btw i had been eating sucrose @ and grains like crazy 90% of my life, now im eating waay less sugar and 0 grains)

  • Anonymous

    4/17/2011 11:57:29 AM |

    edit,

    1:58 > EAT  (not 10:58...)

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