Explains fat burning rate slows down and we regain typically over next 60 months.
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GaleHawkins
Posts: 8,159 Member
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If you're obese. Doesn't apply the same to people who are just overweight. While mitochondrial issues may still lie while someone obese loses weight, fat oxidation can still be achieved.
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Well, I've decided that I'm going to be a special snowflake. This weight IS coming off, and it IS staying off. End of.0
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And yet, people still somehow succeed...0
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Interesting article, Gale - thanks for posting it.
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Here are three quotes near the end of article:
p. 368 "Exercise can slow but but not prevent weight recovery."
p. 369 "Because weight loss is rarely sustained and causes additional impairment of fat oxidations, advice to obese patients to lose weight by curbing calorie intake seems misplaced."
p. 369 "The failure of current clinical recommendations for patients to control their weight through calorie restriction and aerobic exercise are likely due to their adverse affects on mitochondria fat oxidation."
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This paper: http://www.hindawi.com/journals/jl/2013/420754/
Suggests the opposite, that it is mostly Fatty acid over abundance that is the cause of obesity.
"Overall the present data provide evidence that the excess lipid accumulation in non-adipose tissues, including skeletal muscle, of the obese Zucker rat is primarily due to an increased FA availability rather than a major intrinsic impairment in the ability to oxidize fatty acids."
What metabolic difference they found was "cured" my tinkering with CPT1 levels.
"Our ex vivo studies of palmitate oxidation seem to exclude the possibility that this results from a limitation in the capacity of tissues to oxidize FA. A much more likely explanation relates to the known elevation of tissue malonyl-CoA in the obese Zucker rats [40] which may be responsible by suppressing CPT I activity and diverting FA into storage as reviewed by [41]. In support of this, studies in our laboratory using pharmacological ACC inhibition in obese Zucker rats have shown normalization, relative to lean Zuckers, of both hepatic malonyl-CoA levels as well as ability to oxidize FA at the whole-body level (Oakes et al., unpublished observation)."
Which means it is a fatty acid transport-to-mitochondria problem, not a mitochondria problem. A quick jaunt to Wikipedia (I know, I know) shows that this is caused by hyperglycemia and hyper insulinemia. Both of these things are medically treatable and often lifestyle-change treatable (http://en.m.wikipedia.org/wiki/Carnitine_palmitoyltransferase_I)
So which paper is more accurate? Uhhhhhh......
To early to tell I'd wager. Almost everything on this subject is 2008+ so it's new. Here's to learning more!0 -
It is almost like research is done to prove one's initial position vs just doing the research and letting the data fall where it may.
As some of you remember the first of Aug 2014 the rheumatologists told me to read up on Enbrel injections to manage my ankylosing spondylitis and prepare to start on Enbrel after my Nov 2014 appointment.
Cancer was mentioned over and over as I read about Enbrel but I still was planning to start the injections because my ability to even get in and out of cars by myself was quickly declining.
So in my push to learn how to lower the potential of developing cancer or how to treat it after the fact I learned more and more about the theories about the causes of cancer. Of course the Sugar theory popped up and the thought it causes 'inflammation' that can lead to cancer I thought maybe getting off sugar could lower my pain and help lower the risk of cancer.
In short the first of Oct 2014 I went off carbs cold turkey (<50 grams daily) and by Nov 2014 my pain level had dropped from 7-8 to 2-3 on a 1-10 scale so at that appointment I told the rheumatologists I was going to pass on Enbrel injections for now and see how staying off carbs worked out to manage my pain levels.
That went over like a lead balloon and they dismissed me from their clinic that day and said to contact them when I was ready to start on Enbrel.
Since that time I have lost more family to cancer and others have popped up with it so at my age I have stayed with my anticancer research. Asia and Europe seems to be to most advanced in looking beyond surgery, chemo and radiation.
While the research is all over the board it is Vitamin D3 usage that I find the most exciting.
If one will get and keep vitamin D levels in the 60-80 ng/ml range then death from cancer, heart failure and most all causes is greatly reduced until around 100 years of age it seems.0
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