Are You a Hyper-Assimilator?
Peter D'Adamo, ND
Joe and Mike sit down for lunch. Both are about the same age. Joe is a bit shorter and leaner. Mike is a bit taller and heftier. Lunch is buffet style, all you can eat. Joe proceeds to pile up his plate and heartily enjoys his repast, including several slices of bread. Mike skips the bread and selects the lower calorie options and spoons them on his plate with smaller helping sizes. After finishing his first serving Joe heads back to the buffet table and proceeds to fill another plate, which he proceeds to ravish with the same intensity as his first. Next morning, both jump on their scales. Joe is the same weight he always is: 145 pounds. Mike, on the other hand, discovers he has gained another pound and now pushes the scales at 211.
Why do people like Joe seem to never feel satisfied with meals, eat with impunity and yet never seem to gain weight, while others like Mike must watch every calorie and exercise daily and diligently to simply hold to the same weight? New evidence suggests that the differences may be partly genetic and partly environmental.
Many unsuccessful dieters struggle against a set of genetic controls that program their genes for 'metabolic thriftiness.' Just like your thrifty neighbor who can't seem to ever throw anything out, and whose garage is filled with bundles of old newspapers he will never read, thrifty metabolisms are designed to hold onto calories. This may be an ancient survival mechanism, since the ability to lower our metabolism and store all ingested calories as fat would have been a very desirable genetic trait during times of famine and/or unpredictable food supplies. Indeed for most of human history and in most cultures a pear-shaped, fleshy body type would have indicated health, good nutrition and worldly wealth. Our obsession with thinness is a more recent development. Unfortunately a trait like metabolism thriftiness would appear to be more of a liability nowadays in a world where people are much more sedentary and high-caloric foods are cheap and abundant.
Obesity appears in fact as the result of a complicated mix of factors such as genetics, environment, diet, and lifestyle, resulting in an alteration of the equilibrium between energy expenditure and storage.
Not surprisingly, metabolic thriftiness begins in the digestive tract, and
the composition of our gut microflora is increasingly being seen as a potential
factor in human obesity. It is estimated that the human digestive tract may
contain up to 100 trillion microorganisms (1) and the human gut may host up
to 500-1000 different species of bacteria, of which as little as 7% have been
successfully cultured in the laboratory. (2) In the absence of particular intestinal
microbes, the fine blood network (capillaries) of the absorptive machinery
of the small intestinal (villi) fail to develop.
During metabolic diseases such as obesity and diabetes, it has been proposed that an imbalance between the two dominant groups of beneficial bacteria, the Bacteroidetes and the Firmicutes, generates signals controlling the expression of genes by the epithelial intestinal cells.
We still do not know much about why and how gut bacteria induce fat synthesis,
but at least three pathways have been found. (3) Gut microbiota is profoundly
involved in the utilization of ingested nutrients, and obese individuals are
thought to be more efficient in energy extraction from nutrients than lean
individuals. This effect has been demonstrated when researchers inoculated
germ-free mice with a conventional "obese" flora, which led to a significant
weight. It is also known that genetically obese mice harbored a fecal microflora
much more efficient in sugar fermentation and therefore promoting fat deposition.
A 2004 study showed that in one germ-free mouse strain, the mice had 42% less
body fat than conventionally raised mice, even though the conventionally raised
mice ate 29% less food per day. The investigators found that implantation of
adult germ-free mice with a normal microbiota harvested from the distal intestine
(cecum) of conventionally raised animals produced a 60% increase in body fat
content and insulin resistance within 14 days despite reduced food intake.
(4) This huge increase in body fat content was associated with a decrease in
lean body mass.
Interestingly, many of the biochemical markers associated with 'obese flora' improve after gastric bypass surgery, perhaps begging the question of whether gastric bypass actually accomplishes its effects by microbiota reassortment. (5)
Defects in autophagy, a type of 'cellular housekeeping' has been shown to result in greater propensity towards weight gain. Defective autophagy has been already linked to important metabolic disorders such as fatty liver, obesity and atherosclerosis, and the age-dependent decrease in autophagy could underline the basis for the metabolic syndrome of aging. (6)
What To Do If You Are A Hyper-Assimilator
1. Proper Diet
At the very minimum, follow the correct diet for your ABO blood group. Eating
right for your type insures that you are consuming foods that can help to balance
out the bacterial population in your digestive tract. If possible, go the next
step and incorporate the GenoType Diet information, either from the book, Change
Your Genetic Destiny, or by using the SWAMI software system.
formulated from three well-researched botanicals from the traditional texts of
China, India, and Japan and the flavonoids quercetin and resveratrol. Glycoscia supports
the body's natural ability to maintain healthy blood sugar levels. It also may
have anti-glycation end product effects as well.
the herb Salacia oblogna, which has been used for thousands of years in Ayurvedic
medicine. Salacia plays an important role in supporting natural carbohydrate
metabolism and in maintaining the homeostasis of lipid metabolism. (7) The inhibition
of these substances is thought to help the body maintain healthy blood glucose
3. Trehalose Complex
Autophagy ('self-eating') is a catabolic (breakdown) process used by cells to degrade and remove some of their internal components deemed to be unnecessary or undesirable. Our cells are little factories of a sort, and as such they function under many of the same dynamic considerations: Things accumulate and byproducts are produced that can't do anything, etc. Trehalose, a naturally occurring sugar found in most plants helps cells to perform this important function. (8)
4. Other Enhancements
Using the correct probiotic for your blood type can also be an important assist
in regulating the correct microbial balance inside your gut. (9)
Polyflora O | Polyflora
A | Polyflora
B | Polyflora
Blocking the effects of food lectins can also help, since these have been shown to alter the composition of the gut microflora.(10)
Deflect O | Deflect
A | Deflect
B | Deflect
- Bäckhed F, Ley RE, Sonnenburg JL, Peterson DA, Gordon JI. Host-bacterial mutualism in the human intestine. Science. Mar 25; 307(5717):1915-20. (2005)
- Gilbert SF and Epel D. Ecological Developmental Biology. Sinauer Associates. Massachusetts MA USA (2009)
- Bäckhed F, Ding H, Wang T, Hooper LV, Koh GY, Nagy A, Semenkovich CF, Gordon JI. The gut microbiota as an environmental factor that regulates fat storage. Proc Natl Acad Sci U S A. 2004 Nov 2; 101(44):15718-23.
- Bose M, Olivan B, Teixeira J, Pi-Sunyer FX, Laferrere B. Do incretins play a role in the remission of type 2 diabetes after gastric bypass surgery: what are the evidence? Obes Surg. 2008; 19:217?229.
- Singh R, Cuervo AM. Lipophagy: connecting autophagy and lipid metabolism.
Int J Cell Biol. 2012;2012:282041. Epub 2012 Mar 28.
- Li Y, Huang TH, Yamahara J.Salacia root, a unique Ayurvedic medicine, meets
multiple targets in diabetes and obesity. Life Sci. 2008 May 23;82(21-22):1045-9.
Epub 2008 Mar 28.
- Sarkar S, Davies JE, Huang Z, Tunnacliffe A, Rubinsztein DC.Trehalose, a
novel mTOR-independent autophagy enhancer, accelerates the clearance of mutant
huntingtin and alpha-synuclein. J Biol Chem. 2007 Feb 23;282(8):5641-52. Epub
2006 Dec 20.
- Vasconcelos IM, Oliveira JT. Antinutritional properties of plant lectins.
Toxicon. 2004 Sep 15;44(4):385-403.
Are you a calorie Hyper-Assimilator?
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