Calling all super-duper weight losers!






Have you lost at least 1/2 your weight, e.g., 300 lbs down to 150 lbs? If you have, I have a major national magazine editor looking to talk to you.

If you have gone wheat-free and/or followed the dietary advice offered here in The Heart Scan Blog or through the Track Your Plaque program and would be willing to share your story, please let me know by commenting below. While losing half your body weight is not necessarily a requirement for health, it makes an incredibly inspiring story for others.

If we use your story, I will set aside a copy of my soon-to-be-released book, Wheat Belly.

Lp(a): Be patient with fish oil

High-dose omega-3 fatty acids from fish oil has become the number one strategy for reduction of lipoprotein(a), Lp(a), in the Track Your Plaque program for gaining control over coronary plaque and heart disease risk.

The original observations made in Tanzanian Bantus in the Lugalawa Study by Marcovina et al first suggested that higher dietary exposure to fish and perhaps omega-3 fatty acids from fish were associated with 40% lower levels of Lp(a). Interestingly, higher omega-3 exposure was also associated with having the longer apo(a) "tails" on Lp(a) molecules, a characteristic associated with more benign, less aggressive plaque-causing behavior.

Of course, the 600+ fish- consuming Bantus in the study consumed fish over a lifetime, from infancy on up through adulthood. So what is the time course of response if us non-Bantus take higher doses of fish oil to reduce Lp(a)?

We have been applying this approach in the Track Your Plaque program and in my office practice for the past few years. To my surprise, the majority of people taking 6000 mg per day of omega-3 fatty acids, EPA and DHA, will drop Lp(a) after one year.  Some have required two years.  Therefore checking Lp(a) after, say, 3 or 6 months, is nearly useless. (An early response does, however, appear to predict a very vigorous 1-2 year response.)

I'm sure that there is an insightful lesson to be learned from the incredibly slow response, but I don't currently know what it is.  But this strategy has become so powerful, despite its slow nature, that it has allowed many people to back down on niacin.

Baby your pancreas

There it is, sitting quietly tucked under your diaphragm, nestled beneath layers of stomach and intestines, doing its job of monitoring blood sugar, producing insulin, and secreting the digestive enzymes that allow you to convert a fried egg, tomato, or dill pickle into the components that compose you.

But, if you've lived the life of most Americans, your pancreas has had a hard life. Starting as a child, it was forced into the equivalent of hard labor by your eating carbohydrate-rich foods like Lucky Charms, Cocoa Puffs, Hoho's, Ding Dongs, Scooter Pies, and macaroni and cheese. Into adolescent years and college, it was whipped into subservient labor with pizza, beer, pretzels, and ramen noodles. As an adult, the USDA, Surgeon General's office and other assorted purveyors of nutritional advice urged us to cut our fat, cholesterol, and eat more "healthy whole grains"; you complied, exposing your overworked pancreas to keep up its relentless work pace, spewing out insulin to accommodate the endless flow of carbohydrate-rich foods.

So here we are, middle aged or so, with pancreases that are beaten, worn, hobbling around with a walker, heaving and gasping due to having lost 50% or more of its insulin-producing beta cells. If continued to be forced to work overtime, it will fail, breathing its last breath as you and your doctor come to its rescue with metformin, Actos, Januvia, shots of Byetta, and eventually insulin, all aimed at corralling the blood sugar that your failed pancreas was meant to contain.

What if you don't want to rescue your flagging pancreas with drugs? What if you want to salvage your poor, wrinkled, exhausted pancreas, eaking out whatever is left out of the few beta cells you have left?

Well, then, baby your pancreas. If this were a car with 90,000 miles on it, but you want it to last 100,000, then change the oil frequently, keep it tuned, and otherwise baby your car, not subjecting it to extremes and neglect to accelerate its demise. Same with your pancreas: Allow it to rest, not subjecting it to the extremes of insulin production required by carbohydrate consumption. Don't expose it to foods like wheat flour, cornstarch, oats, rice starch, potatoes, and sucrose that demand overtime and hard labor out of your poor pancreas. Go after the foods that allow your pancreas to sleep through a meal like eggs, spinach, cucumbers, olive oil, and walnuts. Give your pancreas a nice back massage and steer clear of "healthy whole grains," the nutritional equivalent of a 26-mile marathon. Pay your pancreas a compliment or two and allow it to have occasional vacations with a brief fast.

Bread equals sugar

Bread, gluten-free or gluten-containing, in terms of carbohydrate content, is equivalent to sugar.

Two slices of store-bought whole grain bread, such as the gluten-free bread I discussed in my last post, equals 5- 6 teaspoons of table sugar:








 

 

 

 

 

 

 

 

Some breads can contain up to twice this quantity, i.e., 10-12 teaspoons equivalent readily-digestible carbohydrate.

Gluten-free carbohydrate mania

Here's a typical gluten-free product, a whole grain bread mix. "Whole grain," of course, suggests high-fiber, high nutrient composition, and health.



 

 

 

 

 

 

 

 

What's it made of? Here's the ingredient list:
Cornstarch, Tapioca Starch, Whole Grain Sorghum Flour, Whole Grain Teff Flour, Whole Grain Amaranth Flour, Soy Fiber, Xanthan Gum, Soy Protein, Natural Cocoa and Ascorbic Acid

In other words, carbohydrate, carbohydrate, carbohydrate, carbohydrate and some other stuff. It means that a sandwich with two slices of bread provides around 42 grams net carbohydrates, enough to send your blood sugar skyward, not to mention trigger visceral fat formation, glycation, small LDL particles and triglycerides.

Take a look at the ingredients and nutrition facts on the label of any number of gluten-free products and you will see the same thing. Many also have proud low-fat claims.

This is how far wrong the gluten-free world has drifted: Trade the lack of gluten for a host of unhealthy effects.

Gluten-free is going DOWN

The majority of gluten-free foods are junk foods.

People with celiac disease experience intestinal destruction and a multitude of other inflammatory conditions due to an immune response gone haywire. The disease  is debilitating and can be fatal unless all gliadin/gluten sources are eliminated, such as wheat, barley, and rye.

A gluten-free food industry to provide foods minus gliadin/gluten has emerged, now large enough to become an important economic force. Even some Big Food companies are getting into the act, like Kraft, that now lists foods they consider gluten-free.

So we have gluten-free breads, cupcakes, scones, pretzels, breakfast cereals, crackers, bagels, muffins, pancake mixes and on and on. All are made with ingredients like brown rice flour, cornstarch, tapioca starch, and potato starch. Occasionally, they are made with amaranth, teff, or quinoa, other less popular, but gluten-free, grains.

Problem: These gluten-free ingredients, while lacking gliadin and gluten, make you fat and diabetic. They increase visceral fat, cause blood sugar to skyrocket higher than nearly all other foods (even higher than wheat, which is already pretty bad), trigger formation of small LDL and triglycerides, and are responsible for exaggerated postprandial (after-eating) lipoprotein distortions. They cause heart disease, cataracts, arthritis, and a wide range of other conditions, all driven by the extreme levels of glycation they generate.

Eliminating all things wheat from the diet is one of the most powerful health strategies I have ever witnessed. But replacing lost wheat with manufactured gluten-free foods is little better than replacing your poppyseed muffin with a bowl of jelly beans.

Whenever we've relied on the food industry to supply a solution, they've managed to bungle it. Saturated fat was replaced with hydrogenated fat and polyunsaturates; sucrose replaced with high-fructose corn syrup. Now, they are replacing wheat gluten-containing foods with junk carbohydrates.

For this reason, I am bringing out a line of recipes and foods that will be wheat gliadin/gluten-free, do NOT contain the junk carbohydrates that gluten-free foods are made of, and are genuinely healthy. They are tasty, to boot.

The gluten-free industry needs to smarten up. Having a following that is free of cramps and diarrhea but are obese, diabetic, and hobbling on arthritic knees and hips is good for nobody.

Medicine ain't what it used to be

The practice of medicine ain't what it used to be.

For instance:

White coats are out-of-date--Not only do they serve as filthy reservoirs of microorganisms (since they hang unwashed after repeated use week after week), they only serve to distance the practitioner from the patient, an outdated notion that should join electroshock therapy to treat homosexuality and other "disorders" in the museum of outdated medical practices.

Normal cholesterol panel . . . no heart disease?

I often hear this comment: "I have a normal cholesterol panel. So I have low risk for heart disease, right?"

While there's a germ of truth in the statement, there are many exceptions. Having "normal" cholesterol values is far from a guarantee that you won't drop over at your daughter's wedding or find yourself lying on a gurney at your nearest profit-center-for-health, aka hospital, heading for the cath lab.

Statistically, large populations do indeed show fewer heart attacks at the lower end of the curve for low total and  LDL cholesterol and the higher end of HDL. But that's on a population basis. When applied to a specific individual, population observations can fall apart. Heart attack can occur at the low risk end of the curve; no heart attack can occur at the high risk end of the curve.

First of all, to me a "normal" lipid panel is not adhering to the lax notion of "normal" specified in the lab's "reference range" drawn from population observations. Most labs, for instance, specify that an HDL cholesterol of 40 mg/dl or more and triglycerides of 150 mg/dl or less are in the normal ranges. However, heart disease can readily occur with normal values of, say, an HDL of 48 mg/dl and triglycerides of 125 mg/dl, both of which allow substantial small oxidation-prone LDL particles to develop. So "normal" may not be ideal or desirable. Look at any study comparing people with heart disease vs. those without, for instance: Typical HDLs in people with heart attacks are around 46 mg/dl, while HDLs in people without heart attacks typically average 48 mg/dl--there is nearly perfect overlap in the distribution curves.

There are also causes for heart disease that are not revealed by the lipid values. Lipoprotein(a), or Lp(a), is among the most important exceptions: You can have a heart attack, stroke, three stents or bypass surgery at age 40 even with spectacular lipid values if you have this genetically-determined condition. And it's not rare, since 11% of the population express it. How about people with the apo E2 genetic variation? These people tend to have normal fasting cholesterol values (if they have only one copy of E2, not two) but have extravagant abnormalities after they eat that contribute to risk. You won't know this from a standard cholesterol panel.

Vitamin D deficiency can be suggested by low HDL and omega-3 fatty acid deficiency suggested by higher triglycerides, but deficiencies of both can exist in severe degrees even with reasonably favorable ranges for both lipid values. Despite the recent inane comments by the Institute of Medicine committee, from what I've witnessed from replacing vitamin D to achieve serum 25-hydroxy vitamin D levels of 60-70 ng/ml, vitamin D deficiency is among the most powerful and correctable causes of heart disease I've ever seen. And, while greater quantities of omega-3 fatty acids from fish oil are associated with lower triglycerides, they are even better at reducing postprandial phenomena, i.e., the after-eating flood of lipoproteins like VLDL and chylomicron remnants, that underlie formation of much atherosclerotic plaque--but not revealed by fasting lipids.

I view standard cholesterol panels as the 1963 version of heart disease prediction. We've come a long way since then and we now have far better tools for prediction of heart attack. Yet the majority of physicians and the public still follow the outdated notion that a cholesterol panel is sufficient to predict your heart's future. Nostalgic, quaint perhaps, but as outdated as transistor radios and prime time acts on the Ed Sullivan show.

 

Idiot farm

The notion of genetic modification of foods and livestock is a contentious issue. The purposeful insertion or deletion of a gene into a plant or animal's genome to yield specific traits, such as herbicide resistance, nutritional composition, or size, prompted the Codex Alimentarius Commission, an international effort to regulate the safety of foods, to issue guidelines concerning genetically-modified foods.

The committee is aware of the concept of unintended effects, i.e., effects that were not part of the original gene insertion or deletion design. In their report, last updated in 2009, they state that:

Unintended effects can result from the random insertion of DNA sequences into the plant genome, which may cause disruption or silencing of existing genes, activation of silent genes, or modifications in the expression of existing genes. Unintended effects may also result in the formation of new or changed patterns of metabolites. For example, the expression of enzymes at high levels may give rise to secondary biochemical effects or changes in the regulation of metabolic pathways and/or altered levels of metabolites.

They make the point that food crops generated using techniques without genetic modification are released into the food supply without safety testing:

New varieties of corn, soybean, potatoes and other common food plants are evaluated by breeders for agronomic and phenotypic characteristics, but generally, foods derived from such new plant varieties are not subjected to the rigorous and extensive food safety testing procedures, including studies in animals, that are typical of chemicals, such as food additives or pesticide residues, that may be present in food.

In other words, conventional plant breeding techniques, such as hybridization, backcrossing, and introgression, practices that include crossing parental plants with their progeny over and over again or crossing a plant with an unrelated plant, yield unique plants that are not subject to any regulation. This means that unintended effects that arise are often not identified or tested. Plant geneticists know that, when one plant is crossed with another, approximately 5% of the genes in the offspring are unique to that plant and not present in either parent. It means that offspring may express new characteristics, such as unique gliadin or gluten proteins in wheat, not expressed in either parent and with new immunological potential in consuming humans.

Dr. James Maryanski, the FDA's Biotechnology Coordinator, stated during Congressional testimony in 1999 that:

The new gene splicing techniques are being used to achieve many of the same goals and improvements that plant breeders have sought through conventional methods. Today's techniques are different from their predecessors in two significant ways. First, they can be used with greater precision and allow for more complete characterization and, therefore, greater predictability about the qualities of the new variety. These techniques give scientists the ability to isolate genes and to introduce new traits into foods without simultaneously introducing many other undesirable traits, as may occur with traditional breeding. [Emphasis mine.]

Efforts by the Codex Alimentarius and FDA are meant to control the introduction and specify safety testing procedures for genetically modified foods. But both organizations have publicly stated that there is another larger problem that has not been addressed that predates genetic modification. In other words, conventional methods like hybridization techniques, the crossing of different strains of a crop or crossing two dissimilar plants (e.g., wheat with a wild grass) have been practiced for decades before genetic modification became possible. And it is still going on.

In other words, the potential hazards of hybridization, often taken to extremes, have essentially been ignored. Hybridized plants are introduced into the food supply with no question of human safety. While hybridization can yield what appear to be benign foods, such as the tangelo, a hybrid of tangerines and grapefruit, it can also yield plants containing extensive unintended effects. It means that unique immunological sequences can be generated. It might be a unique gliadin sequence in wheat or a unique lectin sequence in beans. None are tested prior to selling to humans. So the world frets over the potential dangers of genetic modification while, all along, the much larger hazard of hybridization techniques have been--and still are--going on.

Imagine we applied the hybridization techniques applied by plant geneticists to humans, mating an uncle with his niece, then having the uncle mate again with the offspring, repeating it over and over until some trait was fully expressed. Such extensive inbreeding was practiced in the 19th century German village of Dilsberg, what Mark Twain described as "a thriving and diligent idiot factory."

Eat triglycerides

Dietary fats, from olive oil to cocoa butter to beef tallow, are made of triglycerides.

Triglycerides are simply three ("tri-") fatty acids attached to a glycerol backbone. Glycerol is a simple 3-carbon molecule that readily binds fatty acids. Fatty acids, of course, can be saturated, polyunsaturated, and monounsaturated.

Once ingested, the action of the pancreatic enzyme, pancreatic lipase, along with bile acids secreted by the gallbladder, remove triglycerides from glycerol. Triglycerides pass through the intestinal wall and are "repackaged" into large complex triglyceride-rich (about 90% triglycerides) molecules called chylomicrons, which then pass into the lymphatic system, then to the bloodstream. The liver takes up chylomicrons, removes triglycerides which are then repackaged into triglyceride-rich very low-density lipoproteins (VLDL).

So eating triglycerides increases blood levels of triglycerides, repackaged as chylomicrons and VLDL.

Many physicians are frightened of dietary triglycerides, i.e, fats, for fear it will increase blood levels of triglycerides. It's true: Consuming triglycerides does indeed increase blood levels of triglycerides--but only a little bit. Following a fat-rich meal of, say, a 3-egg omelet with 2 tablespoons of olive oil and 2 oz whole milk mozzarella cheese (total 55 grams triglycerides), blood triglycerides will increase modestly. A typical response would be an increase from 60 mg/dl to 80 mg/dl--an increase, but quite small.

Counterintuitively, it's the foods that convert to triglycerides in the liver that send triglycerides up, not 20 mg/dl, but 200, 400, or 1000 mg/dl or more. What foods convert to triglycerides in the liver? Carbohydrates.

After swallowing a piece of multigrain bread, for instance, carbohydrates are released by salivary and gastric amylase, yielding glucose molecules. Glucose is rapidly absorbed through the intestinal tract and into the liver. The liver is magnificently efficient at storing carbohydrate calories by converting them to the body's principal currency of energy, triglycerides, via the process of de novo lipogenesis, the alchemy of converting glucose into triglycerides for storage. The effect is not immediate; it may require many hours for the liver to do its thing, increasing blood triglycerides many hours after the carbohydrate meal.

This explains why people who follow low-fat diets typically have high triglyceride levels--despite limited ingestion of triglycerides. When I cut my calories from fat to 10% or less--a very strict low-fat diet--my triglycerides are 350 mg/dl. When I slash my carbohydrates to 40-50 grams per day but ingest unlimited triglycerides like olive oil, raw nuts, whole milk cheese, fish oil and fish, etc., my triglycerides are 50 mg/dl.

Don't be afraid of triglycerides. But be very careful with the foods that convert to triglycerides: carbohydrates.

 

 

 

 

 

 

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

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

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

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

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

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

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

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

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

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

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

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

Comments (60) -

  • Anne

    1/19/2010 3:29:13 PM |

    I can attest to the fact that doctors ignore what happens to blood glucose after eating. My fasting BG has always been normal but my glucose tolerance tests have always been high. My last glucose tolerance test a few yrs ago went to 201. My doctors told me I had some insulin resistance but assured me that I did not have to do anything about it because my fasting was OK.

    About 1 year ago, after reading this blog and others, I bought a glucometer. Yes, my fasting was "normal" but I could easily push it up to 200 by eating. I did just what Dr. Davis recommends. I used the glucometer to figure out what I can eat and how much I can eat. I am able to keep my blood glucose below 120 now. The glucometer is a powerful tool.

    Is it possible my ignored elevated post meal blood sugars did damage? Well, lets see, I have peripheral neuropathy and have had cardiac bypass. Giving up gluten 6 yrs ago greatly improved my PN and relieved my of shortness of breath and pitting edema. Getting my blood glucose down will make a difference too.

    I recommend Blood Sugar 101 http://www.phlaunt.com/diabetes/

  • sdkidsbooks

    1/19/2010 5:09:59 PM |

    Going to get a glucose meter today and start checking.  Is there a desirable number or range for glucose before and after or is it about how much or how little it rises without regard to the number?
    Seems like somewhere around a 100 is what you are advocating.  

    If a person is not diabetic, is it helpful at all to know your A1C when getting routine blood work done?  Just wondering...

    Thanks.

    Jan

  • Anonymous

    1/19/2010 6:38:43 PM |

    You can get Wavesense Keynote test strips from Amazon for about 35 cents per strip -- the best deal I've ever seen.  (The meter is about $35 there.)  

    I am curious about the right time to test.  If blood sugar goes to 160 at 30 minutes, but is down to, say, 100 at one hour, is that ok? Why is one hour (not 30 mins or 2 hours) the key number?

  • Gretchen

    1/19/2010 7:02:35 PM |

    Ground meat is often cut with breadcrumbs. I won't eat ground meat or meatloaf at a restaurant or potluck supper.

    Balsamic vinegar contains up to 3 g of glucose per tablespoon. And most people do add sugar to salad dressings. One restaurant I went to boiled down cider vinegar until it was sweet.

    You can use those urine glucose test strips to test foods for the presence of glucose before you eat them. If it's starch, you have to chew the food a bit first to break down the starch. See Richard Bernstein's "Diabetes Solution."

  • Anonymous

    1/19/2010 7:16:36 PM |

    When exactly do you take the measurement?  One hour after the start of a meal or one hour after the end?  Sometimes when we eat out, a meal can take an hour or more to finish.

  • DrStrange

    1/19/2010 7:48:44 PM |

    One caution is that blood sugar meters are only accurate to plus or minus 20% which is a huge variance.  Also, many (probably worst w/ the Walmart Relion or similar budget meters) are not very consistent so you can't just compare to a lab test and calibrate.  

    What I generally do is take 3 (or even 4) readings within a few seconds of each other, toss any wild outliers, then average what is left.  If you try this a few times, depending on your meter, you may be shocked at how much difference there is between the readings.

  • Calvin

    1/19/2010 7:51:01 PM |

    Dr. Davis--Great post--I totally agree. Even if someone isn't diabetic or prediabetic (myself),  investing in a glucose meter, then self-testing (especially post postprandial) has got to be one of the absolute best investments one can make in personal health.

    I once read that if most diabetics (and I'll add prediabetics too) had invested in a meter years before their diagnosis, mostly likely they could have/would have avoided many of their accompanying negative health conditions today.  

    That said, there is still a lot of "cognitive dissonance" with regards to diet and health--I think the meter really helps to reinforce the cognition portion of that phrase thereby reducing the dissonance half.  

    And using a glucose meter can actually be fun!

  • Future Primitive

    1/19/2010 10:33:28 PM |

    Here's an example of carbo loading on yam and plantain - there was a 7 hour "fast" prior to eating and then taking the measurements.

    http://tinyurl.com/bg-set-001

    mg/dL is marked at a few key points on the right hand side.

    What I don't get is how to interpret the second rise and fall after the two hour mark ... though it is still inside the post-absorptive window (which closes 3-5 hours after eating, IIRC).

    I'm pretty certain a glass of red wine explains the initial drop to 65 mg/dL, btw.

    Also, for those that would like to make their own graph, it's easy to grab the url and fill in your own data (it's a google charts thing).

  • notrace

    1/20/2010 12:04:01 AM |

    Will there still be production of small LDL from excess blood glucose even if there is ample available glycogen storage space? That is, will the liver simultaneously manufacture LDL and glycogen?

  • Anonymous

    1/20/2010 2:37:04 AM |

    When do you start to count your one hour.  From the time of your first bite of food, or when you have  finished your last bite.  Since it takes about 20-30 minutes to finish eating, when to start the one hour count down is important.

  • Dr. William Davis

    1/20/2010 2:58:57 AM |

    Hi, Anne--

    What a perfect example of the power of postprandial testing!

    Yes, Jenny Ruhl at http://diabetesupdate.blogspot.com  provides a wealth of insight into blood sugar issues. We will also be releasing an in-depth Special Report on this issue on the www.trackyourplaque.com website.

  • Dr. William Davis

    1/20/2010 3:00:50 AM |

    In answer to the questions on timing of blood sugar checks:

    I am guilty of oversimplification. The peak timing of blood sugar varies on the foods consumed and the mix of foods consumed. It will also vary from individual to individual. I believe a reasonable way to start out is to check 60 minutes from the completion of a meal. Even better, you might occasionally perform your own time-course study: Check blood sugars every 30 minutes to determine when you tend to peak.

  • Coach Jeff

    1/20/2010 12:58:55 PM |

    Since an LC diet causes insulin resistance, (Actually a GOOD and protective thing within the context of an LC diet)wouldn't a long-term low carber get a sort of "false positive" reading of high blood sugar from ANY high carb meal?

    Also, what do you think of the theory (that seems to really be gathering momentum lately) that fructose is the actual cause of insulin resistance, while on a "high carb" diet, and that glucose/starch is relatively benign?

  • Anonymous

    1/20/2010 1:12:53 PM |

    I got a blood glucose monitor after I starting taking niacin for HDL (had read that niacin could raise blood glucose) and it was an eye opener. Now I know what foods to avoid.

    Jeanne

  • Dr. William Davis

    1/20/2010 1:43:47 PM |

    Gretchen--

    Great thoughts. I forgot about the bread crumbs in ground meat issue.

  • Dr. William Davis

    1/20/2010 1:45:17 PM |

    Coach--

    I think it's a matter of degree: While fructose is clearly a very bad player, glucose/starch are not benign, just less bad. Look at the responses we can generate with glucose tolerance testing using 75 grams of glucose.

  • Peter

    1/20/2010 2:55:25 PM |

    Since a simple way to reduce after-meal glucose readings is to eat smaller meals and eat more often, I don't quite understand why you think it's a bad idea.

  • Anonymous

    1/20/2010 3:27:43 PM |

    Bloodsugar101 suggests timing from the start of the meal. I always set a timer anyway, and it is easier to do before beginning to eat than at the end of the meal. This can feel awkward at first in restaurants, but I look at it as a way to get the word out.

    The occasional checks every 30 minutes is an excellent suggestion. Anytime you go over 140, you're causing damage. Even if it is only for brief periods, you want to be sure this is not one of your staple foods!

  • Anonymous

    1/20/2010 8:07:02 PM |

    What has happended to your trackyourplaque forum? I can't reach it anymore? Server crash without any backups? :-(

  • P

    1/20/2010 9:26:25 PM |

    hmmm. How painful is it to check the blood sugar that often?

  • Anonymous

    1/20/2010 10:13:42 PM |

    I'm curious to know how to interpret blood sugar readings on the background of a healthy weight and a low-carb diet, with no known diabetes.  

    My fasting sugar is the same as it was before going low-carb (mid-70s).  However, it now takes a lot fewer carbs to spike my postprandial sugars.  

    An example: after 25 grams of carb in the form of a small serving of sweet potato with butter, my 45 minute postprandial reading, measured in triplicate, was 135.  I'm guessing the peak was even higher.  In case it matters, I'm a 36yo woman with a BMI of 18.9.  

    Should I be unconcerned by this kind of spike as long as my typical meals don't spike my sugar?  Is this just the normal insulin resistance caused by a low-carb diet, as Coach Jeff mentioned in his comment?

  • Anonymous

    1/20/2010 11:06:20 PM |

    Dr. Davis, you said, "While fructose is clearly a very bad player, glucose/starch are not benign, just less bad. Look at the responses we can generate with glucose tolerance testing using 75 grams of glucose."

    This does not prove anything about what causes insulin resistance in the first place though.  The person having a response to glucose during a tolerance test may have originally gotten their insulin resistance from fructose.  You can't use fructose in the test since it doesn't raise blood sugar, you can only use glucose.  

    To put it another way, people who don't have insulin resistance don't have abnormal responses to glucose during glucose tolerance tests.  Does that exonerate glucose?  Not really.  

    What I'm saying is you can't indict glucose OR fructose based solely on what is seen in a glucose tolerance test.

  • Dr. William Davis

    1/21/2010 11:59:56 AM |

    Anon--

    Blood sugars are too high. Either too much carbohydrate in the diet or something has caused an abnormal insulin response. While the dangers are not acute, there are long-term consequences of blood sugars this high.

  • frogfarm

    1/21/2010 3:02:19 PM |

    Dr. Davis, if you can spare a moment I hope you would comment on this:

    http://fanaticcook.blogspot.com/2010/01/should-you-take-vitamin-d2-or-vitamin.html

    where Dr. Michael Holick (Mr. Vitamin D, from the look of his pedigree) claims D2 is equally as effective as D3 in raising and maintaining 25OHD levels?

  • DrStrange

    1/21/2010 3:43:05 PM |

    There are two main causes of insulin resistance, dietary fat and possibly fructose.  Fructose is not a cause for many as they can eat a mostly fruit diet without issues but for some it is a big factor.  There are "must have" essential fatty acids needed in proper amounts and ratio, perhaps a bit more fat is needed.  Beyond that minimum amount, any additional adds to insulin resistance. The amounts and ratios are all present in an all plant diet without the addition of any add oils or fats and that w/ minimal nuts/seeds (maybe an ounce of flax).

    After being on strict McDougall diet (total dietary fat approx 10% and no refined carbs, no animal products, no junk) for about 18 months, I did a 75 gm glucose tolerance test and had them do an extra point at 30 minutes just in case. My highest peak was 114.  Previously, on low carb diet I would go to 185 or higher. [I am 5'3" and 110 pounds so small body mass; lbs body per gm glucose if that makes any difference]

  • TedHutchinson

    1/21/2010 8:49:40 PM |

    @ frogfarm said...
    I find it very strange people take this particular study seriously.

    At the end of the trial none of the participants had 25(OH)D levels above 30ng/ml, so they all remained vitamin D insufficient.
    IMO it is unacceptable medical practice to knowingly give people an amount of a supplement that leaves them at such a low 25(OH)D level they remain unable to properly absorb calcium and well below the 58.8ng/ml level at which human breast milk flows replete with D3.
    So too little vitamin D of any kind leaves you vitamin D deficient.
    Is that such a remarkable finding?

    BUY DISCOUNT Ostoforte 50,000 IU (also called Drisdol) ONLINE 50,000 IU (100 capsules)  $168.99 USD
    or you can choose
    Vitamin D3 $26.95 for 100 X 50,000iu capsules.
    Who, but a fool, chooses to pay $169 when there's a better, cheaper alternative costing only $27?
    Or choosing an oilbased gelcap still saves loads of money.
    Healthy Origins, Vitamin D3, 10,000 IU, 360 Softgels $23.95

    I'm not sure of the point or the common sense, involved in trying to prove a synthetic drug, humans have to convert to D3 anyway, may, in trivial amounts too low to get anybody out of insufficiency, may be as good as a natural, cheaper, product or that equivalence seen in a few persons at a very low dose level, also applies at the sensible, natural levels, desirable for optimum health outcomes.

    While there are cases like this listed in Pubmed it is clear some people do not absorb nor are able to use Vitamin D2.
    We report a case of a 56-year-old woman who received supratherapeutic doses of ergocalciferol (150,000 IU orally daily) for 28 years without toxicity.

    A small trial of just 68 people is unlikely to pick up cases like the above.

    Grassrootshealth Banner Graph shows the amounts people have been taking and the 25(OH)D levels they have achieved.
    6000~8000iu approx 1000iu/daily for each 25lbs you weigh generally produces a natural level at which the body is able to store a sufficient reserve of D3 to be effective at times of crisis.
    This LEF study is another example showing 5000iu/d is not sufficient to get most people above 50ng/ml.

    As Holick knows perfectly well human skin naturally makes 10,000iu/daily given a few minutes full body UVB exposure. It does that for a purpose. Only when researchers start using equivalent EFFECTIVE amounts of the same NATURAL Vitamin D3 biologically identical to the form human skin NATURALLY makes, will we see an improvement rates of chronic illness.

  • Anonymous

    1/21/2010 9:13:05 PM |

    Dr Strange, if you're eating low carb, you have to prep for a GTT by carb-loading for 3-5 days beforehand.  Your pancreas won't be prepared to handle 75g of carb unless you give it a few days to rev up insulin production first.

    The reason that you had no problem with the GTT while McDougalling was that your body was used to high-carb loads, and so the test posed no challenge to your pancreas.

  • TedHutchinson

    1/21/2010 9:33:39 PM |

    Testing in Pairs
    Although this idea is for diabetics I feel it may also be useful for others wanting to see how particular food/exercise choices affect their numbers.
    There is also a short video, a downloadable record form and an example to consider.

  • Anonymous

    1/22/2010 5:22:55 AM |

    I can support what others are saying: before I went low carb, I could eat carbs and my blood glucose would never go above 120; now I eat pretty low carb and a single sweet potato can take me to 150.  I guess one should either eat extremely low carb or extremely high carb to avoid glucose spikes.

  • Dr. William Davis

    1/22/2010 3:04:13 PM |

    I worry that chronically eating high-carbohydrate, while generating an "accommodation" response that blunts postprandial blood sugars, will generate pancreatic BURNOUT by constantly challenging the pancreas to overproduce insulin.

  • Vladimir

    1/22/2010 3:47:56 PM |

    I too find that my post-meal glucose goes up much more after I do have carbs, if I'm eating low carb than high carb.  It's kind of amazing, and a little worry-some.

    However, if I eat very low carb, my fasting glucose is in the low 80s, while if I have more carbs, it's in the high 90s the next morning.  For example, I have (following the blog's advice) had absolutely no wheat and minimal sugar since Dec 27.  My fasting glucose had fallen into the low to mid 80s.  Two days ago, I had a large cookie after lunch --  My first wheat/sugar in 3 weeks.  The next morning, my fasting glucose was 98.

  • DrStrange

    1/22/2010 3:57:49 PM |

    Insulin resistance is the key here and dietary fat is a major contributor to IR.  I simultaneously took insulin levels w/ the blood sugar readings in the 75 gm glucose tolerance test above, and they were consistently low normal to slightly below normal, starting w/ undetectable level at fasting. Readings were:

    fasting < 2
    30 minutes = 3
    60 minutes = 5
    120 minutes = 14
    180 minutes = 8


    reference ranges given on lab report:
    fasting  < 17
    30 minutes = 6-86
    60 minutes = 8-112
    120 minutes = 5-55
    180 minutes = 3-20


    Doesn't seem like too much risk of burn out there!  And again, the reason for the low insulin output generating a fairly flat and low sugar curve was that without excess dietary fat (7-10% of total calories), there is dramatically reduced insulin resistance.

  • Matt Stone

    1/22/2010 6:47:00 PM |

    Thanks for bringing up the importance of blood sugar levels. I've done the same thing with my followers in my recent eBook on type 2 Diabetes, Metabolic Syndrome, and Prediabetes.

    What I have done is take it a step further. Instead of noting what my blood sugar reaction is to a large meal full of high GI starch and trying to avoid it, my focus has been finding ways to improve my glucose tolerance to such a meal.

    My glucose response to food is now far better than any single person following the advice of this blog. That much I can guarantee. It is not luck. It is not genetics. I watched my numbers fall as I followed insights that I gained from several years of intense investigation on the subject.

    The big thing that low-carb authors are missing is that unrefined carbohydrates can improve glucose response to food, even if they cause a larger rise in blood sugar in the short-term.

    My blood sugar now peaks at levels below 80 mg/dl after meals, something that the medical and nutrition-sphere probably considers to be impossible. But it's not. It's glucose metabolism perfection, but it's not achieved through limiting glucose intake. In fact, that can make your response to glucose worse, not better.

  • I Pull 400 Watts

    1/22/2010 9:58:30 PM |

    When you say low carb, what percentage of your calories are coming from carbs? Talking under 30% here?

  • Ateronon

    1/23/2010 6:43:30 AM |

    Off topic here but wish you would discuss salt and its effect on heart disease. There has just been a well publicized news story on it:

    http://www.cnn.com/2010/HEALTH/01/21/salt.intake/

    Do you recommend cutting salt intake to your patients?

    Great blog!

  • DrStrange

    1/23/2010 9:38:02 PM |

    "...if I eat very low carb, my fasting glucose is in the low 80s...  Two days ago, I had a large cookie after lunch -- My first wheat/sugar in 3 weeks. The next morning, my fasting glucose was 98."

    Yes, the high fat content of low-carb diet causes insulin resistance!  If you ate low fat (around 10% total calories max) for a couple weeks then you would maintain the lower fasting sugar after a carb load. Though if that cookie had a lot of fat in it, that could be enough to kick up the insulin resistance again.  One other possibility is if you are gluten intolerant, the stress to your system of eating wheat cookie could make fasting bg higher.

  • Vladimir

    1/24/2010 3:28:38 AM |

    Dr. Strange, Do you have any evidence that a diet high in healthy fats -- I'm a vegetarian, so I get little saturated fat -- causes insulin resistance?  I've never seen that theory propounded, and the mechanism seems implausible to me.

  • Matt Stone

    1/24/2010 5:57:21 PM |

    Dr. Strange-

    Interesting thoughts and you are right to question low-carb dogma as well as to show that insulin resistance is the core problem - and that a very high-fat, low-carb diet worsens the core problem.

    Anyone questioning this has not researched the issue thoroughly enough.


    However, you are making the same mistake. Eating a high-carb, low-fat diet for an extended period of time, while lowering your fasting glucose and insulin levels, also makes your glucose tolerance worse.

    Let me explain...

    If you have a basline meal, let's say, a slab of baby back ribs with cornbread and baked beans, and your 1-hour pp is 140 mg/dl, fasting the next day is 100, then you have good base numbers to track improvement.

    Eat low-carb, high-fat for 10 weeks, eat that same meal (ribs), and both your fasting and pp glucose levels will be higher than they were before you went low-carb. This means you're in worse shape than before the experiment.

    If you eat low-fat, high-carb for 10 weeks, and you eat a slab of ribs, cornbread, and baked beans...
    You're pp and FG will measure into the stratosphere (my 1-hour pp actually hit 173 mg/dl breaking a low-fat escapade...nutritarian).

    Both diets made your glucose metabolism worse in response to your baseline meal.  In other words, both strategies give you better numbers in the interim while making you fundamentally unhealthier (not to mention eating low-fat will make you crave more fat and low-carb will make you crave more carbs).

    What I've found is how to improve your glucose levels and insulin sensitivity in response to normal mixed food ratios. That's where real healing is achieved. A low-carber or a "low-fatter" will never get to a point where he or she can eat a large mixed meal with lots of fat, carbohdyrates, protein, and calories without having high postprandial spikes and high fasting glucose levels. Only someone who can eat 2 baked potatoes with 2T of butter and an 8-ounce untrimmed ribeye with fasting levels in the 70's and pp's in the 70-90 range is truly healthy and free of insulin resistance. I've found the secret to achieving that, and it is not low-fat, low-carb, or low-calorie.

    If such a meal sends your blood sugar half way to Mars, then you need to fix that!  Not avoid it!

  • Anonymous

    1/24/2010 11:32:13 PM |

    @ Matt Stone:

    Stop spamming! Yes, "everyone is wrong but I have figured it all out but for won't tell you what it is unless you go to my web site and pay me" is a spam, plain and simple. Please stop it.

  • DrStrange

    1/25/2010 12:42:19 AM |

    MattStone said: "Only someone who can eat 2 baked potatoes with 2T of butter and an 8-ounce untrimmed ribeye with fasting levels in the 70's and pp's in the 70-90 range is truly healthy and free of insulin resistance."

    That is somewhat how I used to eat and my fasting sugar level was creeping skyward.  Switched to low carb and felt gradually worse and worse for the 9 months I did it.  Switched to low-fat/starch based diet and have been feeling very well and not craving fat at all.  I do eat a little over an ounce per day of flax and pumpkin seeds for EFA boost.

    On 4 different occasions over the past couple years I have sent my blood sugar way up from one meal of moderate fat intake.  One was from eating all the seeds in a medium sized Delicata squash in one meal, maybe 1/2 cup or a bit more.

    Admittedly my liver is not in the best of shape due to much solvent exposure working in surfboard industry years ago and this my contribute...

    Don't have evidence handy but my understanding is that saturated fat is the biggest contributor to IR, much more so than unsaturated. There is some saturated fat in veg foods, some are very high in fact like coconut.

  • DrStrange

    1/25/2010 1:53:35 AM |

    Matt, Have read some on your blog site and think I get the overall picture of what you are doing but...

    What about the demographic data showing increasing cancer rates w/ increasing consumption of animal protein?  And the at least transient damage from meals high in sat. fat?:

    http://content.onlinejacc.org/cgi/content/short/48/4/715
    Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and Endothelial Function
    CONCLUSIONS: Consumption of a saturated fat reduces the anti-inflammatory potential of HDL and impairs arterial endothelial function. In contrast, the anti-inflammatory activity of HDL improves after consumption of polyunsaturated fat. These findings highlight novel mechanisms by which different dietary fatty acids may influence key atherogenic processes.

    And this one is a little concerning (its title tells the tale):
    http://www.ncbi.nlm.nih.gov/pubmed/18263705
    Glucose and leptin induce apoptosis in human beta-cells and impair glucose-stimulated insulin secretion through activation of c-Jun N-terminal kinases.

    More on low fat diet and atherosclerosis:

    http://www.heartattackproof.com/resolving_cade.htm

    It is a fascinating concept that increasing leptin dramatically reduces insulin resistance.  Leptin secretion seems to be induced by increasing glucose level, so eating starch (unrefined carbs like potatoes, whole grains, etc)which converts directly to glucose, should raise leptin level.  What I do not understand is the need for high fat and saturated fat in the diet, nor the need for "overfeeding."  We do need a certain amount of fat in our diets, but a plant based diet, with the addition of an ounce or so of selected seeds/nuts does seem to cover the 10-15% calories from fat we need without the increased disease risks of higher fat intake, and the risks from intake of large amounts of animal protein.

  • billye

    1/25/2010 5:03:20 PM |

    All 42 comments are amazing,

    Lots of varied comments here.  How do you suppose we all arrived here in the first place?  Our genes traveled through the ages,  without the benefit of all of this information.  How did they do this you might ask?  Simple, our ancient ancestors ate what their genes required for survival, full fat wild animal product, supplemented by a few wild not very starchy roots pulled from the ground, and seasonal wild not very sweet tree fruit.  This progressed throughout the last 2.5 million years.  That is how we got here.  Where we went wrong is when agriculture and farming started about 10,000 years ago followed by industry.  Our genes did not change much in the last 2.5 million years of eating high saturated fat including all high fat organs and marrow from the bones, with limited seasonal veggies and fruit.  They did not have the benefit of the sage advice of modern traditional medicine, or electronic devices to guide them, relative to the easy to treat by lifestyle change metabolic syndrome diseases.  Weren't they lucky?  Lest you think I am disparaging all doctors, I am not.  G-d forbid you have a broken leg or a disease that is congenital or inherited  that is difficult or near impossible to treat and need a physician, this group of dedicated highly trained professionals are  a life raft, and much appreciated.  I practice what I preach.  I went from a very ill patient to one that has reversed many of the metabolic syndrome illness that I suffered.  I trust the wisdom of my ancient ancestors and my doctors who practice out of the box evolutionary medicine to guide me.

    Billy E

  • Jared

    1/25/2010 5:04:46 PM |

    The information and anecdotes you provide about various heart disease issues is very interesting and useful. There is a registered dietitian in the Kansas City Area that has produced a series of informational videos about weight loss, nutrition and healthy living that you may be interested in. Here is her latest Nutrition 101 Video Series: http://www.youtube.com/watch?v=7KZCjcCTCOE&feature=related

    Thank you and happy heart month!

  • TedHutchinson

    1/25/2010 5:44:47 PM |

    @ Dr Strange
    Nutrition and Metabolism  Dietary fat research
    Perhaps you haven't yet read the Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease Patty W Siri-Tarino, Qi Sun, Frank B Hu, and Ronald M Krauss, Jan. 2010
    showing there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.

    With reference to Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties
    The mitochondria of people new to consuming coconut oil will not be  adjusted to it. It takes time to acquire appropriate gut flora. A single ingestion of an unfamiliar dietary substance will have different effects from long term use of the same substance.

    Any single trial comparing an omega 6 frequently consumed with a type of saturated fat the general public are not generally accustomed to will fail to spot the long term benefits of MCT (coconut oil, saturated fat) consumption.
    MCTs suppress fat deposition through enhanced thermogenesis and fat oxidation. MCT's preserve insulin sensitivity. MCTs regulate production of adipocytokines (e.g., adiponectin.

  • DrStrange

    1/26/2010 12:37:51 AM |

    Billye, you might want to read these.  It is true that ancestors ate full fat wild game, which is very very lean.  Also, 100% of it ate its natural diet and not corn, soy, and synthetic supplements and drugs.  Also, they most likely ate primarily a lot of starchy roots, leaves, flowers, insects, whatever they could collect and some meat when they could get that.  The meaty, beefy, caveman is a romantic fantasy.  They also did not live very long so degenerative diseases of aging were not an issue

    http://diabetesupdate.blogspot.com/2009/09/lets-not-twist-history-to-support-our.html

    http://diabetesupdate.blogspot.com/2009/11/saying-something-over-and-over-doesnt.html

  • billye

    1/26/2010 2:06:40 PM |

    Dr. Strange,

    The reasons that ancient peoples expired at a relatively young age was because diseases that are cured today through the use of antibiotics such as malaria along with the many natural disasters that occurred throughout the ages account for this fact.  However, what they did not die from were the diseases of the metabolic syndrome that you attribute inaccurately to degenerative diseases of old age. They are brought on by the standard American diet.  The degenerative diseases that you mention are first found in ancient egyptians from about 12,000 years ago after the advent of agriculture.  The patients can do their own trials under the watchful eye and monitored by their doctors.  The plain fact is that when switching to an ancient evolutionary lifestyle most of the diseases of the metabolic syndrome  reverse themselves.  This is being accomplished by thousands of people all over the world today, including my self.  You might read the well documented by clinical trials, Good Calories Bad Calories by G. Taubes, and Trick and Treat by B. Groves.  

    Billy E

  • billye

    1/26/2010 3:30:08 PM |

    DR.Strange,

    This is a P.S.  Archaeologists have found many human bones that had cut marks inflicted by other waring clans, along with the fact that the population of those times was very small compared to today's populations.  This is in contrast to the huge carnivore animal populations that walked the earth devouring humans who were in their food chain.  Also of note was the proven fact that ancient populations prized the fattest parts of the animal, brains, organs, and marrow from the bones etc.

    Billy E

  • donny

    1/26/2010 4:33:37 PM |

    Dr Richard Bernstein is in his mid-70s, and has type I diabetes. His diet is around 30 grams of carbohydrate a day, and he has no fear of saturated fat. It beggars the imagination that a man like him, whose pancreas hasn't produced any of it's own insulin in over half a century, should live to a ripe old age (as a male type one diabetic, he's already done this, and he ain't done yet.), but that the same diet should be deadly to the non-diabetic. Maybe he's lucky; but, before he learned to tightly control his own blood sugars, (and with as little insulin as possible), he suffered all kinds of complications, hardening of the arteries, high triglycerides, low hdl, early kidney disease, etc. I think Dr Bernstein and his patients provide proof of concept for what Dr Davis is trying to accomplish here for those suffering insulin resistance, whether they happen to be diabetic or not.
    Matt, you can't test insulin levels with a glucose meter. You also can't test any possibly progressive damage to glucose homeostasis that *might* be caused by a high everything diet over the course of years or even decades in a matter of weeks or months. Nor can you say flat out that your metabolism has been "healed" by such a diet. Has your system healed, or was it just healthy enough in the first place that over time it was capable of making the hormonal adjustments necessary to function well on a mixed diet? Can everybody make that leap?
    The thing about leptin and insulin resistance... one of the effects of leptin is to decrease the appetite for carbohydrate. (Maybe by increasing ketosis? or at least lipolysis.) It's almost like carbohydrate restriction is built right into the system.;)

  • DrStrange

    1/27/2010 12:22:58 AM |

    "...of note was the proven fact that ancient populations prized the fattest parts of the animal, brains, organs, and marrow from the bones..."

    Proven?  How they do that?

  • Anna

    1/27/2010 5:12:13 AM |

    FYI, a few tips I have picked up in the years I have been testing my BG,

    For the least amount of pain sensation when lancing my finger, I take the blood sample from the *side* of my finger tip, *not* on the pad or the tip.    

    If you have chronially cold hands it can be hard to get a good enough sample.  Wash hands with warm water first, dry well.  Swing arm in a big arc few times if necessary, to force more blood to the hands.  Sometimes my house is a bitt chilly but my car is warm from the sun in the driveway.  A few minutes sitting in the sunny car warms up my hands considerably, making a blood drop easy to get.

    It's ok to slightly "milk" the finger from the palm to the tip once, but with warm hands and a few pre-lancing "swings" (described above), that shouldn't be necessary.  It shouldn't take a lot of "milking" to get a good enough sample.

    There's no need to change the lancet tip for each test sample if you are the only one using the lancet (with clean hands, of course).  In fact, the lancet tips become more comfortable with use.  I change the tip only when it becomes dull and uncomfortable.  It goes without saying the lancet tip should always be changed if it is used to get a blood sample for another person.

    Speaking of clean hands, be sure there is no sugar on your hands or it can affect your results.  Wink

  • TedHutchinson

    1/27/2010 1:04:07 PM |

    @ Anna
    Thanks for tips. I've just started testing (following Dr D's suggestion)
    Bit surprised at some of the numbers.
    5.7=102mg/dl premeal
    8.1=146mg/dl 1hr after meal
    Chicken portion in curry sauce + carrots
    Probably tikka sauce (bought ready meal sugar listed 3rd in marinade and in sauce. Won't buy that again.
    Generally between 6.1 and 6.9 110mg/dl~125mg/dl

  • billye

    1/27/2010 2:20:12 PM |

    Dr. Strange,

    There is so much Paleolithic archaeological proof that ancient populations prized brains, organs, and marrow from bones, that it boggles the mind.  Have you not read about the thousands of bones along with tools found in ancient caves? They were smashed to get at the brains and marrow.  I call your attention to the Quarterly Review Of Biology, Vol 79, No1 March 2004, one of the many studies and reports out there.  Meat eating - dietary shift to increased regular consumption of fatty animal tissues in the course of hominid evolution as mediated by selection for "meat adaptive" genes.  This selection conferred resistance to disease risks associated with meat eating also in life expectancy.  The data was produced at the University of southern California, Los Angeles California.  This argument is long over, unless you wish to ignore all of the indisputable archaeological proof available.  Lets get on with out of the box medicine which supports health.  

    Billy E, nephropal.com

  • The Accidental Farmer

    1/29/2010 12:30:13 PM |

    Coach Jeff said: Since an LC diet causes insulin resistance, (Actually a GOOD and protective thing within the context of an LC diet) . . .

    I am new to this blog, got the link from the Taubes Talk yahoogroups board, and I am curious about this statement.  Why is IR good and protective?  I eat a very high fat diet, as well as low carb, as that is what seems to control my hypoglycemia the best, and so this statement seems counter-intuitive.  Or am I mistaken in thinking that hypoglycemia is a sign that one is developing insulin resistance?  If so, then it would seem that if something relieves the symptoms of hypoglycemia, then it is not leading to further insulin resistance.

  • TedHutchinson

    2/9/2010 3:09:04 PM |

    Following Dr Davis's suggestion I bought a Lifescan Onetouch Ultraeasy from Ebay.
    With too many readings higher than I expected, I needed a better way of recording numbers.
    The people at the freephone number at this link
    Lifescan Onetouch will send a cable and software to load and record your readings quickly and easily directly from the meter together with a simple Quick Start Manual.
    As they don't charge for the disk it's quicker and easier than downloading the software, the cable makes the data transfer from meter even quicker.

    People with different makes of meter may like to download the software anyway and enter their figures manually.
    When you have entered a few days readings, the graphs make it easier to see trends.

  • Ron

    2/11/2010 3:09:33 PM |

    I've always been skeptical about the concept that saturated fat increases insulin resistance and here's an article that addresses that fact directly:

    http://wholehealthsource.blogspot.com/2010/02/saturated-fat-and-insulin-sensitivity.html

  • DrStrange

    2/11/2010 8:01:33 PM |

    "I've always been skeptical about the concept that saturated fat increases insulin resistance..."

    Compared to mono fat, not much if any difference.  Try comparing to very low fat diet ie about 10% of total calories and you will clearly see that fat in and of itself, if too much in diet, will indeed greatly increase IR.

  • Andreas

    2/15/2010 12:57:46 PM |

    Dr. Davis, I followed your advice and bought a glucometer. I got severe cravings from time to time. So last time I could not resist I checked my blood sugar. That was after I ate about 300g of nuts, drank a bottle of red wine and ate a big family chocolate bar. The glucometer showed 86 mg/dl which is within normal range. How is that possible?

    Do you have any further recommendations what to look out for in a case like this? I would really like to find the reason and overcome those cravings. I'm not overweight, in fact more the athletic kind of guy. I started eating paleo/EF about a year ok and am doing mostly great except for the cravings.

    Thank you!
    Andreas

Loading