Some people eat vastly more calories than others. If this discrepancy was converted totally to body fat over a 10 year period, even allowing for some increased energy expenditure, these people would end up as big as a house. But clearly they don't. Mostly. So my question is: where does that excess energy go?
We have things called uncoupling proteins(UCP). There are 5 that have been identified, UCP-1,UCP-2, etc. UCP-1 is present in brown fat and it's what hibernating animals use to keep warm.
Normally, in the mitochondria the ADP is phosphorylated by the electron transport chain and makes ATP (the body's energy currency) and some heat. These UCPs allow this to become 'uncoupled' from ATP production and dissipate completely as heat. This can happen while we sleep and I think explains why some people (like myself) can overeat and wake up really hot and sweaty during the night, and lose up to 4-5 lbs during sleep.
Roles of these proteins are still being discovered/hypothesized. Here are some excerpts from the scientific literature:
At least in rodents, UCP1 seems to be solely responsible for the increase in energy expenditure after cold exposure and sympathetic stimulation. UCP2 and UCP3 are able to uncouple respiration from ATP production and, even though their primary function is not the regulation of energy metabolism, they might still influence energy expenditure as a secondary effect of their physiological function. Several putative functions have been postulated, amongst which are the prevention of ROS production, the regulation of the [ATP]:[ADP] ratio and the regulation of glucose and fatty acid metabolism and fatty acid anion export. (Schrauwen and Hesselink 2002)
In conclusion, it is suggested that UCP3 has an important physiological function in facilitating outward transport from the mitochondrial matrix of fatty acid anions that cannot be oxidized, thereby protecting against lipid-induced mitochondrial damage.(Schrauwen and Hesselink 2004)
T3 increases mitochondrial respiration and promotes, in rodents, the uncoupling between oxygen consumption and ATP synthesis. (Barbe et al. 2001)
These experiments demonstrate that UCP3 is regulated differently in muscle as compared with BAT and suggest that thyroid hormone is a physiologic regulator of UCP3 but not of UCP2... Muscle UCP3 levels were unchanged in ob/ob mice, but leptin treatment of ob/ob mice caused an increase in UCP3 mRNA levels. Muscle UCP2 levels were constant in the three groups. In BAT, both UCP3 and UCP1 were low in ob/ob mice and increased with leptin treatment(Gong et al. 1997).
UCP-2 and UCP-3 Proteins Are Differentially Regulated in Pancreatic Beta-Cells... Both UCP-2 and UCP-3 prevent the reactive oxygen species formation and therefore protect living cells against oxidative stress. Furthermore, UCP-3 plays a physiological role in fatty acid metabolism by exporting fatty acids from the mitochondria. UCP-4 and UCP-5 are expressed mainly in the nervous system.... UCP-2 (and potentially other uncoupling proteins) may be important in the regulation of insulin secretion in health, and may contribute to impaired GSIS in diabetes... UCP-2 expression is increased in rodent islets in response to either chronic high glucose or free fatty acid concentration exposure and diabetic human islets.... Therefore, low UCP-3 levels may contribute to the pathogenesis of type-2 diabetes. (Li et al. 2008).
In addition, assuming a role for UCP2 in the regulation of ROS production, a low level of UCP2 expression would increase ROS production, which is particularly dangerous in the case of diabetes because recent data indicate that ROS production is the link between elevated glucose levels and hyperglycaemic damage... In fact, overexpression of UCP1 in endothelial cells reduced ROS production and prevented hyperglycaemic damage (Nishikawa et al., 2000).
Together, these tissue-dependent differential mRNA expressions of the UCP homologues in IBAT, gastrocnemius, and soleus muscles during food deprivation and refeeding are much more consistent with a role for UCP2 and UCP3 in the regulation of lipids as fuel substrate rather than as mediators of regulatory thermogenesis (Samec et al. 1998).
We have recently shown that, in humans, 60 h of mild cold exposure reduced skeletal muscle UCP3 mRNA expression (Schrauwen et al., 2002b), excluding a major role for UCP3 in cold-induced adaptive thermogenesis. Another condition in which UCP3 expression does not reflect the changes in energy expenditure is fasting, during which energy expenditure drops and UCP3 mRNA expression increases both in rodents (Boss et al., 1998b) and in humans (Millet et al., 1997).
The fasting-induced upregulation of UCP3 and subsequent downregulation of UCP3 (below baseline levels) during refeeding provide further evidence that UCP3 is, in fact, more involved in fatty acid metabolism than in energy metabolism (Samec et al., 1999a). Also, the upregulation of UCP3 mRNA expression after acute exercise (Pilegaard et al., 2000) could be attributed to increased metabolic rate and increased fat oxidation in the post-exercise period.
Regardless of their primary functions, UCPs dissipate energy as heat and allow us to regulate our metabolic rate.
edit: for a good review of UCP3, I'd suggest this: http://www.ncbi.nlm.nih.gov/pubmed/15294045
or this for UCP2 and UCP3 http://jeb.biologists.org/content/205/15/2275.full
You're all right!
I can't speak scientifically as Jeff did, but I have observed in my 6 decades that slender people tend to be fidgety and restless so they are in motion more. They may act enthusiastic about food, but if you pay attention many of them eat very tiny portions and leave more food on their plate than they eat.
My dad, now, was 5'6" and weighed 133 lbs all the time--not 130, not 135, he definitely had a set-point of 133. He clearly had abnormal metabolism because he ate like an NFL lineman. He'd eat 2 heaping plates of food plus bread/rolls and he'd have room for dessert. He also didn't metabolize alcohol normally; he could drink a ton and never get drunk (I inherited that aspect and I don't drink because there's no buzz.) He never complained of any digestive issues until he was diagnosed with T2 diabetes in his late 50s. Even then, he ate a ton of food and stayed the same weight without any insulin--he just needed to watch his sugar intake.
In my case (underweight, wiry person from a thin family); I only stop moving/fidgeting when I am sleeping, and I also seem to have a great deal of brown fat which burns off 'extra' as heat rather than adding soft tissue to my frame.
I've always been skinny and hyperactive, but since eating paleo, high calorie and high fat, and healing a lot of health issues, my 'fast metabolism' is more noticeable and extreme. When I ate a shitty grain-based diet, I actually tended to be cold and had a lot of hypothyroid symtoms, but still never gained weight.
The heat I output after overeating, especially from my upper torso, is incredible - you can feel it with your hand a foot away from me sometimes. In the hotter parts of the summer I have to intentionally restrict calories, because this process will make me sweat profusely and even get heatstroke symptoms in temps when most people are comfortable.
I don't believe I have any malapsorption issues. First of all, my shit is not only normal but ideal - if you are truly not digesting food, it will show in your stool. Also I am generally healthy and look it, am never ill, and easily gain strength and endurance - just not mass, especially not fat mass.
BBC TV showed a 1 hour documentary a while back called "Why Are Thin People not Fat". here's an overview of it: http://news.bbc.co.uk/2/hi/uk_news/magazine/7838668.stm
you can find it on you-tube in 7 parts. make sure you search for "Why Are Thin People not Fat" to get the right one.
here's some text from the link above to give you an idea of what its about;
"Why, for example, do some people seem to eat what they like and not put on weight, while others limit their diet yet struggle to shed their bulk?
In 1967, a medical researcher, Ethan Sims, carried out an experiment at Vermont state prison in the US. He recruited inmates to eat as much as they could to gain 25% of their body weight, in return for early release from prison.
Some of the volunteers could not reach the target however hard they tried, even though they were eating 10,000 calories a day. Sims's conclusion was that for some, obesity is nearly impossible.
It was with this in mind that 10 slim volunteers - who were not dieters - convened in more hospitable circumstances, for a recent experiment devised by the BBC's Horizon documentary. The 10 spent four weeks gorging on as much pizza, chips, ice cream and chocolate as they could, while doing no exercise, and severely limiting the amount they walked."
i will not add anything else, as i say it was an hour long program & would not do it justice. you really have to watch it for yourself (if you have the bandwidth).
They may be eating a lot of calories, but they're not absorbing them. I'd say that all the skinny people who eat as much as they want are passing a lot of the calories they eat through, without them being absorbed.
High metabolism with hypothyroid? 1 Answer