Look no farther than Discovery Channel to learn how humans were meant to eat.
The Survivorman show documents the (self-filmed) 7-day adventures of Les Stroud, who is dropped into various remote corners of the world to survive on little but ingenuity and will to live. Starting without food or water, the Survivorman scrapes and scrambles in the wilderness for essentials to survive in habitats as far ranging as the Ecuadorian rainforest to sub-arctic Labrador.
What does Survivorman have to do with your nutrition habits?
Everything. The lessons we can learn by watching this TV show are plenty.
Survivorman plays out the life we are supposed to be living: slaughtering wild game with simple handmade tools and his bare hands, identifying plants and berries that are safe to eat, trapping fish, scavenging the kill of other predators. He's even resorted to eating bugs and caterpillars, particularly following several days of unsuccessful hunting and scavenging.
What is notable from the Survivorman experience is what is absent: In the steppe, desert, tundra, or jungle, you will not find bread, fruit drinks, or Cheerios. You won't find farm-fattened, corn-fed livestock with meat marbled with fat.
Imagine the result of such an experience for us, drawn out over 6 months. Even an obese, diabetic, gluttonous, XXX dress size 350-lb woman would return a lean 105 lbs, size 0, non-diabetic, fully able to run miles in the wild tracking game.
Survivorman's quiet desperation of living in the wild, preoccupied with worries over where his next meal might be found, is a stark contrast to the bloated, shelves stacked floor-to-ceiling supermarkets, and our modern society's all-you-can-eat several times per day lifestyle.
Am I advocating selling the car and house and chucking modern society for the "safety" of the jungles of Borneo?
No, of course not. I am advocating taking a lesson from the clever experiment conducted by Mr. Stroud, a return-to-the-wild experience that should teach us something about how perverse our modern nutritional lives have become.
Carbohydrate intolerance comes in many shades and colors, shapes and sizes.
I call all of its varieties the Carbohydrate Intolerance Syndrome, or CIS. (Not to be confused with CSI, or Crime Scene Investigation . . . though, come to think of it, perhaps there are some interesting parallels!)
At its extreme, it is called type II diabetes, in which any carbohydrate generates an extravant increase in blood sugar, followed by the domino effect of increased triglycerides, reduction in HDL, creation of small LDL, heightened inflammation, etc. and eventually to kidney disease, coronary atherosclerosis, neuropathies, etc.
An intermediate form of carbohydrate intolerance is called metabolic syndrome, or pre-diabetes. These people, for the most part, look and act like diabetics, though their reaction to carbohydrate intake is not as bad. Blood sugar, for instance, might be 125 mg/dl fasting, 160 mg/dl after eating. The semi-arbitrary definition of metabolic syndrome includes at least three of the following: HDL <40 mg/dl in men, <50 mg/dl in women; triglycerides 150 mg/dl or greater; BP 135/80 or greater; waist circumference >40 inches in men, >35 inches in women; fasting glucose >100 mg/dl.
This is where the conventional definitions stop: Either you are diabetic or have metabolic syndrome, or you have nothing at all.
Unfortunately, this means that the millions of people with patterns not severe enough to match the standard definition of metabolic syndrome are often neglected.
How about Kevin?
Kevin, a 56 year old financial planner, is 5 ft 7 inches, 180 lbs (BMI 28.2). His basic measures:
But take a look at his underlying lipoprotein patterns (NMR):
LDL particle number 2231 nmol/L (equivalent to a "true" LDL of 223 mg/dl) Small LDL 1811 nmol/l Large HDL 0.0 mg/dl
In other words, small LDL constitutes 81% of all LDL particles (1811/2231), a severe pattern. Large HDL is the healthy, protective fraction and Kevin has none. These are high-risk patterns for heart disease. These, too, are patterns of carbohydrate intolerance.
Foods that trigger small LDL and reduction in healthy, large HDL include sugars, wheat, and cornstarch. Kevin is carbohydrate-intolerant, although he lacks the (fasting) blood sugar aspect of carbohydrate intolerance. But he shows all the underlying lipoprotein and other metabolic phenomena associated with carbohydrate intolerance.
We could also cast all three conditions under the umbrella of "insulin resistance." But I prefer Carbohydrate Intolerance Syndrome, or CIS, since it immediately suggests the basic underlying cause: eating carbohydrates, especially those that trigger rapid and substantial surges in blood sugar.
CIS is the Disease of the Century, judging by the figures (both numbers and humans) we are seeing. It will dominate healthcare in its various forms for many years to come.
The first treatment for the Carbohydrate Intolerance Syndrome? Some would say the TZD class of drugs like Avandia. Others would say a DASH or TLC (American Heart Association) diet. How about liposuction, twice-daily Byetta injections, or even the emerging class of drugs to manipulate leptin and adiponectin? How do "heart healthy" foods like Cheerios and Cocoa Puffs fit into this? (Don't believe me? The American Heart Association says they're heart healthy!)
The first treatment for the Carbohydrate Intolerance Syndrome is elimination of carbohydrates, except those that come from raw nuts and seeds, vegetables, occasional real fruit (not those green fake grapes), wine, and dark chocolates.
Maggie had been doing well on her program, enjoying favorable lipids near our 60-60-60 targets (HDL 60 mg/dl or greater, LDL 60 mg/dl or less, triglycerides 60 mg/dl or less). Last fall, her last set of values were:
In other words, holiday indulgences caused an increase in LDL cholesterol, a reduction in HDL, an increase in triglycerides, an increase in total cholesterol.
What happened?
At first glance, many of my colleagues would interpret this as fat indulgence and/or a "need" for statin drug therapy.
Having done thousands of lipoprotein panels, I can tell you that, beneath the surface, the following has occurred:
--Overindulgence in carbohydrates from the goodies triggered triglyceride (actually VLDL) formation in the liver, released into the blood. --Increased triglycerides and VLDL triggered a boom in conversion of large LDL to small LDL (since triglycerides are required to form small LDL particles) via cholesteryl-ester transfer protein (CETP) activity. --Increased triglycerides and VLDL interacted with HDL particles, causing "remodeling" of HDL particles to the less desirable, less protective small particles, which do not persist as long in the blood, resulting in a reduction of HDL.
The critical factor is carbohydrate intake. This triggered a domino effect that is often misintepreted as excessive fat intake or a genetic predisposition. It is nothing of the kind.
I discussed this phenomenon with Maggie. She now knows to not overindulge in the holiday snacks in future and will revert promptly back to her 60-60-60 values.
--lack of sunlight/vitamin D/indoor habitation --mental stress --more mental stress --sleep deprivation... (excessive mochas/lattes at Berkeley cafes) --excessive 'social' calendar --inherent family history of autoimmune disorders (who doesn't??) --wheat, wheat, and more wheat ingestion ('comfort foods' craved in times of high cortisol/stress, right? how did I know the carbs were killing me?) --lack of nutritious food containing EPA DHA, vitamin A, sat fats, minerals, iodine, etc --lack of play, exercise, movement (or ?overtraining perhaps for Oprah's case) --weight gain -- which begins an endless self-perpetuating vicous cycle of all the above (Is it stressful to balloon out for no apparent reason? YES)
If you haven't done so already, take a look at Animal Pharm you will get a real kick out of Dr. BG's quick-witted take on things.
We are systematically looking for low thyroid (hypothyroidism) in everyone and findings oodles of it, far more than I ever expected.
Much of the low thyroid phenomena is due to active or previous Hashimoto's thyroiditis, the inflammatory process that exerts destructive effects on the delicate thyroid gland. It is presently unclear how much is due to iodine deficiency in this area, though iodine supplementation by itself (i.e., without thyroid hormone replacement) has not been yielding improved thyroid measures.
I find this bothersome: Is low thyroid function the consequence of direct thyroid toxins (flame retardants like polybrominated diphenyl ethers, pesticide residues in vegetables and fruits, bisphenol A from polycarbonate plastics) or indirect toxins such as wheat via an autoimmune process (similar to that seen in celiac disease)?
I don't know, but we've got to deal with the thyroid-destructive aftermath: Look for thyroid dysfunction, even in those without symptoms, and correct it. This has become a basic tenet of the Track Your Plaque approach for intensive reduction of coronary risk.
