29 replies to this topic

[lucid]

Background:

I'm going to be doing the equivalent of this study (Conjugated linoleic acid supplementation reduces adipose tissue by apoptosis and develops lipodystrophy in mice) on myself.

 

The driving idea behind this experiment is that body weight is metabolically regulated and that effect is mediated by insulin, leptin and some other signalling molecules. When we lose weight, fat cells get smaller, but they dont die. (article) The number of fat cells you have is pretty important because we are coming to understand fat functions like a gland --- releasing regulatory hormones in addition to storing and releasing fat. This is important because when we diet, the number of fat cells doesn't strink, instead fat cells get smaller... and small fat cells stop releasing leptin which is an appetite suppressant among other effects. This makes our weight go back up after a diet.

 

The trick with the above study is that CLA appears to cause apoptosis - killing fat cells instead of them just shrinking. This may reset the 'set point' for body weight regulation. There is a big problem though in doing this --- instead of the fat just going away, it gets re-routed to your liver. Mice in the above study had HUGE livers - like 4x the size of controls. To avoid this side effect, i'm going to take a very high dose of CLA while fasting.

 

Question On Dosing:

What I'm not sure of is how to translate the mouse CLA dose to humans. In the study, CLA (a lipid) made up 2% of the mice' diet by calories. My average metabolic rate is 3500-4000+ KCal (I'm tall with lots of muscle), so for me that's 80 Calories of CLA. A 1 gram pill has 10 calories but it is 80% CLA... So 80 calories is 80/10/0.8 = 10 pills. (@ 1g of 80% CLA per pill) What I wanted to check with you folks is if there is some metabolic scaling from mice to people with CLA? - i know there usually is scaling with pharmaceuticals but am not so sure about CLA.

 

Experiment Details:

I'm 240 (@ roughly 17-19% bodyfat) - will be getting a body scan tom morning for an accurate measurement in the morning

That means I have ~45 lbs of fat.

I'd like to get to 8% body fat as my new set point which would be 16 lbs of fat.

This would mean i need to lose 29 lbs of fat.

To prevent lipodystrophy, i will be fasting or near fasting (@ 0-400 Cal/ Day) and with a metabolic rate of 3500 (conservatively), i will be burning 3,000 calories a day.

Since I will be working out and taking BCA's and because fasting is largely muscle sparing after 3 days, I'm hoping that my lean mass loss is limited to 5 lbs.

This means that in total i need to lose 34 lbs, and at 3200 cal / pound while burning 3000 calories / day, it should take me 36 days to hit target weight.

However after stopping the fast and supplementation, i will have fewer but empty fat cells. My body will then proceed (i expect) to refeed until I then have fewer full fat cells.

What this means is that my weight will go up potentially a good bit maybe 50% increase in fat - as my remaining cells fill back up. That would put me at 12% body fat, which is not the target.

I could then do another round to get lower, but i dont want to do that.

Instead I think I'm going to try to get to 6% bodyfat and then move back up to 8-9% as the fat cells fill back up.

This means that I need to lose another 4lbs of fat and another 1lb of lean mass. That would turn my 36 day adventure into a 42 day adventure.

This means my target weight loss is 39 lbs or getting to 6% bodyfat which ever comes first.

At that point I will have lost 6 lbs of lean mass going from 195 -> 189. And I will have lost 33 lbs of fat mass going from 45 -> 12. WIth my total weight changing from 240 to 201.

 

To track lipodystrophy i will have medical supervision and get ultrasounds. I'll also do extensive blood work before and after.

Ideally id like to biopsy tiny bits of fat and do apoptosis TUNEL staining to see if im getting the desired effect, but this is tricky. Any lab rats here know more about this? Who would i get to do this for me? Or would i just have to buy the kit from a lab supply company?

 

I'd like to make a video about it and share it with the internet if successful.

 

Cheers. all. If you can help with the question above about metabolic scaling -- I would be super appreciative.

[gamesguru]

there would be scaling, but the fact that it is measured as a percentage of diet means it already includes the metabolic or allosteric scaling factor in the calculation. a 50g rat may eat 6g of dry food in a day, but a 50kg girl may have trouble reaching even 1kg. thus, the conversion factor of 6 is already included in the calculation, when we take the dose as a percentage of diet by mass. so it does not make sense to divide again by 6, as this would take you below 20kcal of CLA... an utterally trivial amount.

here's another article that explains interesting cases where commonly accepted "scale-factors" are not to be used, becausing overriding biological factors:
http://www.ncbi.nlm....les/PMC2737649/

Edited by gamesguru, 01 June 2016 - 01:57 PM.

[lucid]

What an excellent answer! Thank you

there would be scaling, but the fact that it is measured as a percentage of diet means it already includes the metabolic or allosteric scaling factor in the calculation. a 50g rat may eat 6g of dry food in a day, but a 50kg girl may have trouble reaching even 1kg. thus, the conversion factor of 6 is already included in the calculation, when we take the dose as a percentage of diet by mass. so it does not make sense to divide again by 6, as this would take you below 20kcal of CLA... an utterally trivial amount.

here's another article that explains interesting cases where commonly accepted "scale-factors" are not to be used, becausing overriding biological factors:
http://www.ncbi.nlm....les/PMC2737649/

 

[gamesguru]

it could be safe to consume even closer to 200kcal daily.

any idea on the CLA content of Kerrygold butter, or of New Zealand ground beef and cheese? i didnt find any info

Edited by gamesguru, 01 June 2016 - 02:30 PM.

[lucid]

Yeah the more i read on long term fasting - the more sure I am that it will be 200-400 Calories a day for me.

 

The CLA content of butter is 5mg / g of fat. It is suggested that summer grass fed dairy products have 4x the CLA of winter or grain fed dairy products. So that might be as high as 20mg / g. I'm not going to get 10 grams of the stuff eating butter

it could be safe to consume even closer to 200kcal daily.

any idea on the CLA content of imported Kerrygold butter, or of ground grassfed New Zealand beef?

 

[gamesguru]

even if I managed 4Tbsp butter, 6oz cheese, and 8oz beef...? which is close to double my average

[lucid]

at 20 mg of CLA / g of fat. you would need 50g of fat to get 1 g of cla. That would be 450 calories of fat. Not bad if part of your diet potentially. That said CLA is a double edged sword with lipodistrophy - so calorie restriction at the same time as supplementation seems important if you want the fat killing effect.

[gamesguru]

I don't think any calorie restriction is needed for the reduced catabolic load, aka muscle loss.

it also has a host of other benefits, like anti-inflammatory or anti-carcinogenic. unless there's oxidation or glycation as a side effect (which, this isnt a CR thread!!), there are plenty of athletic people who could enjoy these benefits without CR.

yeah it is part of my diet, thanks. im just illustrating one of the perks of a grass-fed diet.

Edited by gamesguru, 01 June 2016 - 03:37 PM.

[Logic]

IIRC the Dasatinib kills off senescent adipose progenitor cells. 

http://www.longecity...ds-healthspan/`

So it may be an adjunct to your idea.

 

I worry about killing of fat cells around the eyes etc and  ending up with that sickly, sunken look?

 

[lucid]

Good thought. It isnt like it is going to happen over-night. If my face starts getting ugly ill probably stop shortly there after - during the weight gain afterwards it should reverse some.

 

Also the fat loss should be pretty evenly distributed through the body, so i should lose facial fat at the same rate as i lose other fat. We will see

[lucid]

Also, Dasatinib is like a 350 a day chemo drug

 

So far CLA is the only thing ive seen that triggers adipose apoptosis - anyone seen anything else?

IIRC the Dasatinib kills off senescent adipose progenitor cells. 

http://www.longecity...ds-healthspan/`

So it may be an adjunct to your idea.

 

I worry about killing of fat cells around the eyes etc and  ending up with that sickly, sunken look?

 

 

[gamesguru]

 

Green tea polyphenol epigallocatechin gallate inhibits adipogenesis and induces apoptosis in 3T3-L1 adipocytes.
Lin J1, Della-Fera MA, Baile CA. (2005)
OBJECTIVE:
Green tea catechins have been shown to promote loss of body fat and to inhibit growth of many cancer cell types by inducing apoptosis. The objective of this study was to determine whether epigallocatechin gallate (EGCG), the primary green tea catechin, could act directly on adipocytes to inhibit adipogenesis and induce apoptosis.
RESEARCH METHODS AND PROCEDURES:
Mouse 3T3-L1 preadipocytes and mature adipocytes were used. To test the effect of EGCG on viability, cells were incubated for 3, 6, 12, or 24 hours with 0, 50, 100, or 200 microM EGCG. Viability was quantitated by MTS assay. To determine the effect of EGCG on apoptosis, adipocytes were incubated for 24 hours with 0 to 200 microM EGCG, then stained with annexin V and propidium iodide and analyzed by laser scanning cytometry. Both preadipocytes and adipocytes were also analyzed for apoptosis by terminal deoxynucleotidyl transferase dUTP nick-end labeling assay. To determine the effect of EGCG on adipogenesis, maturing preadipocytes were incubated during the 6-day induction period with 0 to 200 microM EGCG, then stained with Oil-Red-O and analyzed for lipid content.
RESULTS:
EGCG had no effect on either viability or apoptosis of preconfluent preadipocytes. EGCG also did not affect viability of mature adipocytes; however, EGCG increased apoptosis in mature adipocytes, as demonstrated by both laser scanning cytometry and terminal deoxynucleotidyl transferase dUTP nick-end labeling assays. Furthermore, EGCG dose-dependently inhibited lipid accumulation in maturing preadipocytes.

 

Epigenetic effects of green tea polyphenols in cancer
Susanne M Henning, Piwen Wang, Catherine L Carpenter, and David Heber (2014)
Epigenetics describes heritable alterations of gene expression and chromatin organization without changes in DNA sequence. Both hypermethylation and hypomethylation of DNA can affect gene expression and the multistep process of carcinogenesis. Epigenetic changes are reversible and may be targeted by dietary interventions. Bioactive compounds from green tea (GT) such as (–)-epigallocatechin gallate have been shown to alter DNA methyltransferase activity in studies of esophageal, oral, skin, Tregs, lung, breast and prostate cancer cells, which may contribute to the chemopreventive effect of GT. Three out of four mouse model studies have confirmed the inhibitory effect of (–)-epigallocatechin gallate on DNA methylation. A human study demonstrated that decreased methylation of CDX2 and BMP-2 in gastric carcinoma was associated with higher GT consumption. It is the goal of this review to summarize our current knowledge of the potential of GT to alter epigenetic processes, which may be useful in chemoprevention.

 

Green Tea Catechins Inhibit Vascular Endothelial Growth Factor Receptor Phosphorylation
Sylvie Lamy, Denis Gingras, and Richard Béliveau (2002)
Vascular endothelial growth factor (VEGF) receptors (VEGFR) play a major role in tumor angiogenesis and, thus, represent attractive targets for the development of novel anticancer therapeutics. In this work, we report that green tea catechins are novel inhibitors of VEGFR-2 activity. Physiological concentrations (0.01–1 μm) of epigallocatechin-3 gallate, catechin-3 gallate, and, to a lesser extent, epicatechin-3 gallate induce a rapid and potent inhibition of VEGF-dependent tyrosine phosphorylation of VEGFR-2. The inhibition of VEGFR-2 by epigallocatechin-3 gallate was similar to that induced by Semaxanib (SU5416), a specific VEGFR-2 inhibitor. The inhibition of VEGFR-2 activity by the catechins displayed positive correlation with the suppression of in vitro angiogenesis. These observations suggest that the anticancer properties of green tea extracts may be related to their inhibition of VEGF-dependent angiogenesis.

 

 

quercetin, and more:

http://www.ncbi.nlm....pubmed/18979154
http://www.fasebj.or...pplement/602.11
http://www.ncbi.nlm....pubmed/16178781
http://www.ncbi.nlm....pubmed/17039455
http://www.academicj...1_Bin et al.pdf
http://ads.uga.edu/d...415-4222010.pdf

[lucid]

 

 

Green tea polyphenol epigallocatechin gallate inhibits adipogenesis and induces apoptosis in 3T3-L1 adipocytes.
Lin J1, Della-Fera MA, Baile CA. (2005)
OBJECTIVE:
Green tea catechins have been shown to promote loss of body fat and to inhibit growth of many cancer cell types by inducing apoptosis. The objective of this study was to determine whether epigallocatechin gallate (EGCG), the primary green tea catechin, could act directly on adipocytes to inhibit adipogenesis and induce apoptosis.
RESEARCH METHODS AND PROCEDURES:
Mouse 3T3-L1 preadipocytes and mature adipocytes were used. To test the effect of EGCG on viability, cells were incubated for 3, 6, 12, or 24 hours with 0, 50, 100, or 200 microM EGCG. Viability was quantitated by MTS assay. To determine the effect of EGCG on apoptosis, adipocytes were incubated for 24 hours with 0 to 200 microM EGCG, then stained with annexin V and propidium iodide and analyzed by laser scanning cytometry. Both preadipocytes and adipocytes were also analyzed for apoptosis by terminal deoxynucleotidyl transferase dUTP nick-end labeling assay. To determine the effect of EGCG on adipogenesis, maturing preadipocytes were incubated during the 6-day induction period with 0 to 200 microM EGCG, then stained with Oil-Red-O and analyzed for lipid content.
RESULTS:
EGCG had no effect on either viability or apoptosis of preconfluent preadipocytes. EGCG also did not affect viability of mature adipocytes; however, EGCG increased apoptosis in mature adipocytes, as demonstrated by both laser scanning cytometry and terminal deoxynucleotidyl transferase dUTP nick-end labeling assays. Furthermore, EGCG dose-dependently inhibited lipid accumulation in maturing preadipocytes.

 

Epigenetic effects of green tea polyphenols in cancer
Susanne M Henning, Piwen Wang, Catherine L Carpenter, and David Heber (2014)
Epigenetics describes heritable alterations of gene expression and chromatin organization without changes in DNA sequence. Both hypermethylation and hypomethylation of DNA can affect gene expression and the multistep process of carcinogenesis. Epigenetic changes are reversible and may be targeted by dietary interventions. Bioactive compounds from green tea (GT) such as (–)-epigallocatechin gallate have been shown to alter DNA methyltransferase activity in studies of esophageal, oral, skin, Tregs, lung, breast and prostate cancer cells, which may contribute to the chemopreventive effect of GT. Three out of four mouse model studies have confirmed the inhibitory effect of (–)-epigallocatechin gallate on DNA methylation. A human study demonstrated that decreased methylation of CDX2 and BMP-2 in gastric carcinoma was associated with higher GT consumption. It is the goal of this review to summarize our current knowledge of the potential of GT to alter epigenetic processes, which may be useful in chemoprevention.

 

Green Tea Catechins Inhibit Vascular Endothelial Growth Factor Receptor Phosphorylation
Sylvie Lamy, Denis Gingras, and Richard Béliveau (2002)
Vascular endothelial growth factor (VEGF) receptors (VEGFR) play a major role in tumor angiogenesis and, thus, represent attractive targets for the development of novel anticancer therapeutics. In this work, we report that green tea catechins are novel inhibitors of VEGFR-2 activity. Physiological concentrations (0.01–1 μm) of epigallocatechin-3 gallate, catechin-3 gallate, and, to a lesser extent, epicatechin-3 gallate induce a rapid and potent inhibition of VEGF-dependent tyrosine phosphorylation of VEGFR-2. The inhibition of VEGFR-2 by epigallocatechin-3 gallate was similar to that induced by Semaxanib (SU5416), a specific VEGFR-2 inhibitor. The inhibition of VEGFR-2 activity by the catechins displayed positive correlation with the suppression of in vitro angiogenesis. These observations suggest that the anticancer properties of green tea extracts may be related to their inhibition of VEGF-dependent angiogenesis.

 

 

quercetin, and more:

http://www.ncbi.nlm....pubmed/18979154
http://www.fasebj.or...pplement/602.11
http://www.ncbi.nlm....pubmed/16178781
http://www.ncbi.nlm....pubmed/17039455
http://www.academicj...1_Bin et al.pdf
http://ads.uga.edu/d...415-4222010.pdf

 

 

Thanks. I was already thinking about EGCG because I thought I had seen things about it before, but didnt have my fingers on the studies. Any idea on what an effective dose is to get apoptosis?
 

[gamesguru]

it says 100 μM, and EGCG has a molar mass of 458.372, so for a 70kg man we have ( 70 kg ) ( 100e-6 mol/kg ) ( 458.372 g/mol ) = 3.2g

Edited by gamesguru, 02 June 2016 - 11:41 PM.

[niner]

it says 100 μM, and EGCG has a molar mass of 458.372, so for a 70kg man we have ( 70 kg ) ( 100e-6 mol/kg ) ( 458.372 g/mol ) = 3.2g

 

People have damaged their livers with much lower doses than this (of GTE).  There are a lot of problems with converting an in vitro result to a human therapy.  If you stuck with a reasonable dose, it might help some, but I wouldn't expect miracles.

 

 

Also, Dasatinib is like a 350 a day chemo drug

 

It's a lot less when you buy it in powder form on the grey market.  It's a kinase inhibitor, not an old-school chemo drug, so it won't make your hair fall out.  Also, you don't need to take it forever if your goal is to induce senescent cells to go apoptotic.  It's more like a once-and-done therapy.  More realistically, you might do a course once a year or so if you're old enough, like over 55-65 or so.  I wouldn't expect much of a result in a young person.

[gamesguru]

yes, but another study has reported similar effects at one tenth the dose! according to these authors, nothing above 1 micromolar is feasibly attainable in the human subject.

 

(-)-Epigallocatechin-3-gallate blocks 3T3-L1 adipose conversion by inhibition of cell proliferation and suppression of adipose phenotype expression.
Chan CY1, Wei L, Castro-Muñozledo F, Koo WL. (2011)

AIMS:
A major objective in the treatment of obese individuals is the development of agents that reduce body fat and improve metabolic homeostasis. Among a variety of biological effects, green tea exerts an anti-obesity effect; however, the mechanisms behind its activity on adipose tissue are uncertain. Tea contains high levels of (-)-epigallocatechin-3-gallate (EGCG), which is one of its main bioactive substances. Therefore, we studied the effects of EGCG on mouse embryonic fibroblast-adipose like cell line (3T3-L1) preadipocyte proliferation and differentiation.
MAIN METHODS:
3T3-L1 cells were incubated with physiologically attainable (0.1-1 μM) and pharmacological (5μM, 10μM) concentrations of EGCG for various lengths of time. Cell proliferation was assessed by cell counting and cell cycle analysis. Adipose conversion was evaluated by lipid accumulation and expression of CCAAT/enhancer binding protein alpha (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ) transcription factors.
KEY FINDINGS:
A dose dependent suppressive effect on preadipocyte proliferation was observed, with the highest reduction in cell number at 10μM EGCG. On the other hand, adipose conversion was fully inhibited with 10μM EGCG. Flow-cytometric analysis showed that 3T3-L1 cells treated with EGCG underwent an arrest of cell cycle at G2/M. The inhibition of the expression of C/EBPα and PPARγ was accompanied by the inhibitory effect of EGCG. Microscopic observation showed that 3T3-L1 cells treated with EGCG maintained the fibroblastic shape and failed to accumulate cytoplasmic fat droplets even after the induction of differentiation.
SIGNIFICANCE:
Our results suggest that EGCG reduces adipogenesis through an arrest of cell cycle and a blockage of adipose phenotype expression. These results also suggest that the anti-obesity activity of green tea may be partially attributed to its suppressive effects in adipogenesis.

 

[lucid]

Got my body fat scan results yesterday; Turns out I'm fatter than i thought! Im 22.7% fat according to that machine. Yikes!

 

The update to my plan means i need to lose 45 lbs which seems kind of nuts. Should take 2 months now.

[gamesguru]

aye mate. just eat more fiber less fat, and exercise.

[stefan_001]

Perhaps less drastic methods would be good to try first? Fisetin is quite safe.

 

http://www.timelessl...-treat-obesity/

They found that fisetin inhibits lipid accumulation and suppresses the expression of PPARg in 3T3-L1 cells. Fisetin suppressed early stages of preadipocyte differentiation, and induced expression of Sirt1.

[Logic]

aye mate. just eat more fiber less fat, and exercise.

 

Eating fat does not = being fat. Carbs are the problem. Especially processed, high GI carbs.

Easily oxidised and oxidised fats are bad.

[gamesguru]

yes but the important thing is more fiber. as compares dates with coconuts, i prefer the nutritional profile of dates, despite their sugar content

[lucid]

I'm vegitarian / almost vegan - i eat shit tons of fiber, don't drink anything with sugar in it. For being vegitarian, I have a rather low carb diet -> beans, green vegies, tofu or protien supplements and healthy oils.

 

My body is just comfortable around 240; I'm strong (bench 250, squat 350, dead lift 450, ~12 pull ups, 20+ dips) and look pretty good. I have been tracking my weight for the past 5 years in a spreadsheet as I worked out more to put muscle on, counted calories etc. Looking at it -> my body has a certain amount of fat it feels comfortable with -- I can count calories to get below that, but when i lose focus (even with eating the right kinds of foods) it returns to there.

 

This is an effort to totally reset the set point that my body feels comfortable at.

Edited by lucid, 04 June 2016 - 11:28 PM.

[lucid]

Interesting, I'm interested in adipose apoptosis more than adipogenesis. Though perhaps they could both lead to the same end depending on adipocyte turnover rate.

Perhaps less drastic methods would be good to try first? Fisetin is quite safe.

 

http://www.timelessl...-treat-obesity/

They found that fisetin inhibits lipid accumulation and suppresses the expression of PPARg in 3T3-L1 cells. Fisetin suppressed early stages of preadipocyte differentiation, and induced expression of Sirt1.

 

 

[stefan_001]

 

Interesting, I'm interested in adipose apoptosis more than adipogenesis. Though perhaps they could both lead to the same end depending on adipocyte turnover rate.

Perhaps less drastic methods would be good to try first? Fisetin is quite safe.

 

http://www.timelessl...-treat-obesity/

They found that fisetin inhibits lipid accumulation and suppresses the expression of PPARg in 3T3-L1 cells. Fisetin suppressed early stages of preadipocyte differentiation, and induced expression of Sirt1.

 

Very slow, if I recall well about 8 years. Still it may be a good path. Fisetin seems safe and has multiple benefits. Also you may want to look at supplements that tighten glycemic control. For example NR is shown to improve glucose tolerance and reduces weight gain. There are more substances with such effects.

 

It reads as if you have really good discipline I could imagine that with such discipline of reduces calories + supplement stack results should become visible in some months to a year and if not you can always try your method next . Fast killing of fat cells sounds somewhat risky especially as the same earlier mentioned 8 years also applies to restoring them if you go too far (and then there are those liver aspects).

Edited by stefan_001, 05 June 2016 - 07:17 AM.

[Gern]

After reading this, I'm considering something similar but less radical. Keep my calorie consumption around 1800 calories a day, and burn 3000 calories a day through resistance training and aerobic exercise, so I lose around 2lbs a week. Then add CLA, though I have no idea how much. I already take ECGC, NR, and quite a few other things. It would take a six months or so to reach my ideal weight, but if it does indeed reset my 'set point' it would be a worthwhile experiment.

Edited by Gern, 05 September 2016 - 08:58 PM.

[Logic]

 

it says 100 μM, and EGCG has a molar mass of 458.372, so for a 70kg man we have ( 70 kg ) ( 100e-6 mol/kg ) ( 458.372 g/mol ) = 3.2g

 

People have damaged their livers with much lower doses than this (of GTE).  There are a lot of problems with converting an in vitro result to a human therapy.  If you stuck with a reasonable dose, it might help some, but I wouldn't expect miracles.

 

 

Also, Dasatinib is like a 350 a day chemo drug

 

It's a lot less when you buy it in powder form on the grey market.  It's a kinase inhibitor, not an old-school chemo drug, so it won't make your hair fall out.  Also, you don't need to take it forever if your goal is to induce senescent cells to go apoptotic.  It's more like a once-and-done therapy.  More realistically, you might do a course once a year or so if you're old enough, like over 55-65 or so.  I wouldn't expect much of a result in a young person.

 

 

It's good to see you still giving sage advice when people are about to do something ill informed Niner.

IIRC:

750 mg of EGCG in one sitting is the absolute limit, but one can take more if the doses are nicely spread out.
Taking it with food helps protect the liver for some reason?
 

Thx for the maths Gamesguru.

[Lufega]

Hi Lucid,

Any updates on your trial with ClA?

I used cla 3-4 months ago and while initially, I noticed some weight loss I also started to feel tired and unwell. In addition, i believe cla affected my libido and energy levels permanently. Blood tests also showed and elevation in ldl cholesterol and triglycerides. A problem I didnt have before. In short, i experienced the prooxidant effect of CLA and feel it made me unhealthier.

Seeing as its a lipophilic substance it probably still remains in my body which is why I still feel unwell.

Any idea how to undo this other than time?

[Gern]

Hi Lucid,

Any updates on your trial with ClA?

I used cla 3-4 months ago and while initially, I noticed some weight loss I also started to feel tired and unwell. In addition, i believe cla affected my libido and energy levels permanently. Blood tests also showed and elevation in ldl cholesterol and triglycerides. A problem I didnt have before. In short, i experienced the prooxidant effect of CLA and feel it made me unhealthier.

Seeing as its a lipophilic substance it probably still remains in my body which is why I still feel unwell.

Any idea how to undo this other than time?

I did several things at once:
Took CLA - 3000mg twice a day
Ate fewer calories - about 1500 a day
Switched to low carb - 30 g or less a day
Added exercise - about 300 cal a day of weight training & arobic
Added intermittent fasting close to 16/8

Lost a lot of weight fast 33 lbs in a little over two months
It was the easiest weight loss I've ever had - occasional hunger but it never lasted
I was in ketosis most of the time
I had significant strength gains - went from squats using 180 lbs to 220 lbs
The combination of high weight low reps. intermittent fasting and low carb seemed to do wonders to manage appetite

Here's the thing though. I doubt it will have lasting results, nor do I think it will do anything significant to my set point.
Research seems to support several well established facts (I don't have time to dredge up all the studies)

1) Fat produces leptin so the less fat you have the less leptin you produce
2) Leptin suppresses long term hunger so the less leptin you have the the more hungry you become
3) Leptin is sensed in the hypothalamus which signals hunger
4) The exact mechanism is not well understood at this time.

There are many theories. The most knteresting to me involves Nrf2 and ATG4/ATG5. I don't pretend to fully understand them:

https://www.ncbi.nlm...pubmed/28228267
https://www.ncbi.nlm...pubmed/28213613

The bottom line is if you loose significant weight regardless of how, whether through smaller adipose cells or fewer, you will produce less leptin, and your body will want to restore that weight to maintain energy homeostasis. Research does seem to support the idea that you can reduce the number of some types of adipose cells using CLA, but it seems likely the lower leptin levels will just trigger long term hunger that urges you to pack all that weight back in again.

[Logic]

$ 8.93 per gram:
http://www.longecity...m-nyles/page-11

Dosage: 30-100 mg for 1-2 days once or twice a year.

 
 

 

Also, Dasatinib is like a 350 a day chemo drug

 

So far CLA is the only thing ive seen that triggers adipose apoptosis - anyone seen anything else?

IIRC the Dasatinib kills off senescent adipose progenitor cells. 

http://www.longecity...ds-healthspan/`

So it may be an adjunct to your idea.

 

I worry about killing of fat cells around the eyes etc and  ending up with that sickly, sunken look?

 

 

Edited by Logic, 13 March 2017 - 09:42 PM.

[SearchHorizon]

It is probably NOT a good idea to resort to CLA.  CLA damages adipocytes in ways one's body can't cope.

 

Adipocytes that you have are there for a reason. It is not just a storage tissue, but active one that protects your body in many ways.

Because of this, it is not a good idea to directly affect the adipocyte survival and function (i.e., liposuction, CLA administration, etc.).

 

An indirect approach is better (e.g., exercise, diet, and supps that have partitioning effect on nutrients).