1. Metabolism is not genetic.
Clearly, this is not the case. Do not mistake something that is alterable or that can be affected by external influence to not have a genetic component that can affect the outcome or influence initial states or subsequent results. Everything from adipose distribution, fiber expression, mitochondrial activity, endocrinology, histochemistry, and anything else that might have an influence in weight gain/loss has a genetic precursor attached to it. Saying that an individual's metabolism is not genetic is the same as saying that someone's eye color is not genetic either. This isn't an argument of whether hard work will change a person's body composition, but to acknowledge
all factors.
2. Body Type is not genetic.
Excellent...please tell me which exercises I need to do therefore to help me to grow taller, since I would really love to be around 6' tall. Also, please tell me which exercises I will need to do to correct my structural genu varus, my flat feet, and to make my hands a little bigger (it would be a lot easier to palm a basketball after I get taller).
50 years ago there was not an obesity epidemic. There was not the very large proportion of fat kids. (I mention fat kids because if these things are genetic then there would be a similar proportion of fat to skinny kids, there is not) Why?? Because people were more active, and portion sizes were smaller. That is it.
By that same logic, then with the decline of activity levels, there would not be a very large proportion of thin kids now, and while the percentage of children classified as "overweight" has increased 3x from the amount in 1963-1970, this is still "only" an increase from 5% to 16% of the total 12-19 year old population, according to the statistics provided by the CDC/NCHS, which does not support your argument. While the decline in activity levels are among the chief reasons cited for the youth obesity rise, to claim that is the only factor is, again, completely ignoring the multitude of other factors, not to mention demonstrating an ignorance of the role of genetic factors and the current statistical evidence. The argument is not whether or not body type can be affected despite pre-existing genetic factors, which it clearly can be, but whether or not these factors may impact results or ease of body composition change, as well as the influence of body weight in altering existing individual histochemistry to reduce the body's disposition towards weight loss through insulin resistance, leptin resistance, etc, etc.
Metabolism is simply a factor of activity level, as is body type. Anyone that says anything different is kidding themselves.
Well, perhaps I'd like to kid you with some of these sources that claim otherwise:
Genetics of obesity in adult adoptees and their biological siblings.BMJ. 1989 January 14; 298(6666): 87–90.
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In conclusion, though human fatness is influenced by the environment, as shown by differences between monozygotic twins7 and rapid changes over time in stable, homogeneous populations,25 it is clearly under substantial genetic control. The transmission appears to be independent of sex. We suggest that at least two modes of genetic inheritance are concerned-namely, polygenic inheritance for the full range of fatness and a
major gene, or genes, specific for obesity."
Genetics of Obesity: Review Article American Journal of PharmacoGenomics. 2(3):177-187, 2002.
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The most common forms of obesity are polygenic. Two general approaches have been used to date in the search for genes underlying common polygenic obesity in humans. The first approach focuses on selected genes having some plausible role in obesity on the basis of their known or presumed biological role. This approach yielded putative susceptibility genes with only small or uncertain effects. The second approach attempts to map genes purely by position and requires no presumptions on the function of genes. Genome-wide scans identify chromosomal regions showing linkage with obesity in large collections of nuclear families. Genome-wide scans in different ethnic populations have localized major obesity loci on chromosomes 2, 5, 10, 11 and 20. Susceptibility gene(s) for obesity may be positionally cloned in the intervals of linkage."
Genetics of Human Obesity: Recent Results from Linkage Studies The Journal of Nutrition Vol. 127 No. 9 September 1997, pp. 1887S-1890S
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On the basis of these data, and others that cannot be reviewed here, we have recently revised the human obesity gene map as of October 1996 (Pe´russe et al. 1997). The human gene map incorporates the loci from single-gene mutation rodent models of obesity, all QTL from crossbreeding experiments, all relevant Mendelian disorders that have been mapped to a chromosomal region, and genes or markers that have been shown to be associated or linked with an obesity phenotype (Pe´russe et al. 1997)."
Obesity in the New Millennium Nature Vol. 404, 6 APRIL 2000
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Why then are some individuals obese and others not? It seems that the intrinsic sensitivity to leptin is variable and that, in general, obese individuals are leptin-resistant3,14,15. A smaller subset of individuals seems to produce too little leptin. In principle, genetic, environmental
and even psychological factors could influence leptin sensitivity or leptin production. The molecular basis for leptin resistance has been explained in some instances. Leptin acts on nerve cells in the brain and modulates their function (Fig. 2). Several key molecules in this neural network are brain peptides known as neuropeptide Y (NPY)and agouti-related protein (AGRP), which stimulate food intake, and -melanocyte-stimulating hormone (-MSH) and cocaine- and
amphetamine-regulated transcript (CART), which decrease food intake (see review by Schwartz et al., pp. 661–671, and refs 2, 16, 17). These neural circuits also regulate energy expenditure by means of effects on several key molecules that have recently been identified (see review by Lowell and Spiegelman, pp. 652–660). These effectors include uncoupling proteins and peroxisome proliferator-activated receptor- (PPAR-) co-activator-1 (PGC-1), a key regulator of the
genes that control thermogenesis18. Genetic evidence indicates that leptin regulates energy balance by modulating the balance among the aforementioned (and other) neuropeptides4. Mutations in proopiomelanocortin (POMC), the precursor of -MSH, are associated with obesity19. In ~3–5% of extremely obese individuals, mutations in an MSH receptor (MC4R) result in a defect in MSH signalling, which causes leptin resistance18,20,21. Mutation in the leptin receptor is
also associated with extreme obesity22. In other cases it has been suggested that defective transport of leptin across the blood–brain barrier is the cause of leptin resistance and obesity3,23. Several other factors undoubtedly influence the function of this neural network,
and the identification of additional molecules that comprise the neural system will shed more light on the molecular basis of obesity and leptin resistance."
Current understanding of the etiology of obesity: genetic and nongenetic American Journal of Clinical Nutrition, Vol 53, 1561S-1565S
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The data at this point suggest that when energy intake is held at the same level above baseline, two main classes of factors appear to be involved in determining the changes in body mass for a given genotype. These factors are schematically illustrated in Figure 1, which represents a modification of the paradigm that we presented several years ago (5). It would seem from the overfeeding study summarized here that nutrient partitioning (proneness to gain fat or fat-free tissues) is the single most important factor to explain the individuality in body mass gain. Chances are that a significant proportion of those prone or resistant to obesity find themselves in this vulnerable or desirable position because of inhented or acquired differences in nutrient partitioning mechanisms.
This factor in addition to a low resting metabolic rate per unit of fat-free mass and a low level of lipid oxidation relative to carbohydrate oxidation are emerging as the three most useful predictors of weight gain. More longitudinal data are needed on these and other potential determinants of weight gain and
obesity."
The genetics of obesity: from genetic epidemiology to molecular markers. Mol Med Today. 1995 Apr;1(1):45-50
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Obesity is a highly prevalent disease that carries enormous human and economic costs in western nations. The complexity and diversity of the paths leading to an overweight or an obesity status are enormous."
More complicated than initially thought Lipids. 2003 Feb;38(2):97-101
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Despite an obesigenic environment, humans have great variability in their susceptibility to obesity, which is determined in large part by genetics. Current evidence suggests that genetic susceptibility to human obesity is the result of multiple genes, each with a modest effect, that interact with each other and with environmental provocations. Elucidation of obesity susceptibility genes through genome-wide and candidate gene approaches provides great promise in ultimately determining the genetic underpinnings of obesity. "
The reason it is harder for an "endomorph" to lose weight is that they have more than likely been eating too much and doing very little activity for a long time.
Although this may certainly be a huge factor, there are also other factors at work, as evidenced above, that may also contribute beyond too much eating, not enough exercising. We accept that there are genetic factors that predispose us to nearly every disease that can be found today, from diabetes and heart disease to Cancer and Alzheimer's disease. There is evidence for genetic factors impacting other eating disorders as well, including anorexia nervosa, too; why not then another "disease," namely obesity?
I also have personal experience with all body types. I started as an "ectomorph" (5'10" 100lbs) then trained myself to be a "mesomorph" (5'10" 250lbs) then gained to be a "endomorph" (5'10" 330lbs) then became a "mesomorph" (5'10" 205lbs) now my body type would be considered "endomorph." (5'10" 280lbs)
If I choose to, I will change my "body type" again. It is simply behavior that governs metabolism and body type.
I'm sure that your n=1 population sample is excellent evidence to refute the overwhelming evidence of genetic factors in weight gain/loss in the literature, I'm not terribly convinced that there are
no genetic factors involved, or that the genetic factors that may be present are
easily influenced by willpower alone. This is not to negate the effect of hard work and effort (I make half of my living by emphasizing these factors, as do you), it
is to point out that ignoring relevant factors and hurdles to success, ultimately leading to a lack of understanding of the topic or a limited understanding, will skew the success of effectively dealing with the issue.
I have also seen many other people change their "body type" over time. They just did what it took to make it happen.
I have seen people that did everything "right" but still had exceptionally more difficulty in achieving their goals than have others with the same motivation and activity levels. Again, this is not an argument of whether or not proper exercise and diet can make a difference:
clearly it does, and it's such a ridiculous argument to make that I'm not even sure why it needs to be brought up in the first place: this is an attempt to discuss the influence of genetics, which again clearly
does influence a person's "starting point" and ultimate ease of change and success. It's not a question of "if" but of "how" as in "how do we minimize the impact of genetics and maximize results" which is a multi-disciplinary problem with numerous factors and influences, hardly the least of all being genetics.
You know what, it is hard to gain muscle, lose fat, or get in shape, it is not limited to any type of body that someone may think they have. It is not limited to the type of metabolism people have.
Some things are easier for certain individuals while other things are easier for others. We see this casually every day: my girlfriend is naturally inclined towards mathematics while I have to work harder at learning math; my classmate is a sponge when it comes to physiology and pathophysiology while I can barely recall basic concepts; I can "see" vector lines and force diagrams when analyzing movement while my other classmate struggles at even basic biomechanical concepts. We all have natural "strengths and weaknesses" that are influenced not only by our surroundings but that are heavily influenced by natural inclinations that has everything to do with neuronal chemistry and networks, physiological and morphological differences, as well as neuromuscular considerations, too. Why is it so hard to believe that weight loss or weight gain have a similar variability as well? After all, we fully accept that strength, power, coordination and athleticism are genetically influenced...why not body weight?
It takes discipline, consistency, and time. (the amount of each thing will be different for different people, some need to be more consistent, some will take more time, some will require more discipline it all depends upon how well people adapt to habit change)
That would seem to support the argument that myself and others are making: not that obesity can
not be affected, but that some individuals will have a more difficult time in doing so than others...it is not much of a stretch to extend that to the point where an individual, despite "best efforts" will fall short of an ultimate mark or that his/her body will be genetically predisposed to reverting to former bf levels despite adherence to activity levels or diet. This doesn't mean that it is hopeless, just that this possibility needs to be understood and respected for long-term success.
Sure genetics play a role to a certain extent, not as big of a role as people think.
Too general of a statement: for some this may be true, for others this falls far short of the truth and disregards factors that will compromise success. This is evidenced through the literature, anecdotal evidence, and endocrinology/biochemistry theory alike.
