Increased Fat Oxidation (FAO) Does Not Lead To Weight / Fat Loss

[Hans]

Do you have an opinion on what a reasonable dosing schedule would be?

Between 200-400mg depending on bodyweight. Dose could be a bit higher but lower dose is safer.
About 5mg/kg is about average.

 

[Adrienlcrx]

Hi @jb116 what K2 do u use when you saw an improvement on liver health? Kuinone? One drop topical application maybe?

 

[Scenes]

Fats from a meal only appear in the blood about 2 hours after the meal has been eaten so you should be fine.
Muscles burn fat at rest and should help get rid of the fat. Also the liver helps get rid of the PUFAs.

The problems comes in when you deprive yourself of carbs and then increase the oxidation of fat through stress.

Is this implying we should never eat even sat fats alone without sugar? I’m eating more cocoa butter at night (people keep saying eat your fats at night - not exactly sure why). Also not sure whether to have a bit of fruit or sugar with it, as people keep saying combing fat and sugar is bad. Can you explain? Simple question I’m sure.

 

[bdawg]

Probably the other hidden variable is the composition of fat in an organism. May be why some lose weight with increased FAO and get away with it relatively unscathed is less pufa in their tissues. At any rate higher metabolism and oxidative sugar burning is a much better solution ultimately.

DNP? Ah! I say caffeine FTW

caffeine promotes lipolysis and FFA oxidisation - so the benefit is likely via other mechanisms

Caffeine ingestion stimulates both lipolysis and energy expenditure.
After ingestion of caffeine, oxidative FFA disposal increased 44% (236 ± 21 to 340 ± 16 μmol/min), whereas nonoxidative FFA disposal increased 2.3-fold (455 ± 66 to 1054 ± 242 μmol/min; P < 0.01). In postabsorptive conditions, 34% of lipids were oxidized and 66% were recycled. Caffeine ingestion increased energy expenditure 13% and doubled the turnover of lipids, of which 24% were oxidized and 76% were recycled. β-Adrenoceptor blockade decreased, but did not inhibit, these variables.

Metabolic effects of caffeine in humans: lipid oxidation or futile cycling?

 

[LeeLemonoil]

good old ascorbic acid seems to stimulate fat-burning in muscles

Lose weight faster with vitamin C

 

[Steve]

So what method of fat loss is most common among the bodybuilder-types that seem to be able to get very lean & stay that way? I think they all follow a similar method, but I'm not sure exactly what that is.

 

[Hans]

Is this implying we should never eat even sat fats alone without sugar? I’m eating more cocoa butter at night (people keep saying eat your fats at night - not exactly sure why). Also not sure whether to have a bit of fruit or sugar with it, as people keep saying combing fat and sugar is bad. Can you explain? Simple question I’m sure.

It depends on your glycogen stores, but Peat mentioned that you can go about 16-24 hours without carbs if you have good glycogen stores. But if you deplete all your glycogen stores, one big meal will most likely not replenish it, especially if you lift weights as well. So no, I don't imply that carbs should always be eaten with fat, but most likely with protein.
I'm also not sure why someone wants to eat more fat at night, but I think a nice protein and carb meal before bed can be a good idea, especially if you lift weights. Protein before bed increases the metabolic rate the following day.
Combining sugar and fats ain't bad, but if someone has already elevated lipolysis and FFAs, adding extra fat to carbs might have a negative effect on glucose oxidation, especially if calories are eaten in excess. But this also depends on your metabolic rate and how much calories your body uses.

You'll have to experiment with different carb sources and dosages to see what you do best with. Peat advises about a glass or two of OJ before bed, so that could be a good start.

 

[Hans]

So what method of fat loss is most common among the bodybuilder-types that seem to be able to get very lean & stay that way? I think they all follow a similar method, but I'm not sure exactly what that is.

Most bodybuilders use caloric deficit, cardio, sometimes fasted, and then use stimulants like the ECA stack, etc. You never really know what those top guys are using, especially those that claim to be natty but most of them do it the stressful way and just use anabolic and thyroid hormones to try to negate the negatives.

 

[Obi-wan]

Want to lose fat take Orlistat with every meal and the monster FAO inhibitor Mildronate

 

[milkboi]

Want to lose fat take Orlistat with every meal and the monster FAO inhibitor Mildronate

Dang Orlistat sounds crazy... have you ever tried it?

 

[Obi-wan]

Dang Orlistat sounds crazy... have you ever tried it?

If you eat fat while you take Orlistat you will poop it out as an orange oil (sorry) Currently taking it with every meal but I am also trying to eat low fat so I don't have the orange mess. You can buy it at Walmart under the name Alli here in the US. Mildronate works by blocking Carnitine forcing the mitochondria to use Glucose instead of FAO. You can order it on Amazon Prime.

 

[Obi-wan]

The study below directly contradicts a mantra commonly repeated in nutrition circles - restrict glucose and increase fat oxidation in order to lose body fat. In fact, this idea is so ingrained into the minds of most people that I often get hate mail from people all over the world angrily admonishing me that without increasing fat oxidation weight loss will become impossible.
Well, I suggest carefully reading the study below. First, it shows that FAO is independent of energy expenditure. This directly suggests that FAO has a role that is not so much about supplying energy but likely more as a signalling mechanism - i.e. a stress signal. As such, you'd expect increasing the stress signal (in this case FAO) to NOT lead to weight loss. The study found that increasing FAO by 30%+ did not lead to any weight/fat loss. What it did do is decrease glucose oxidation by the exact same percentage as the increase in FAO, thus confirming nicely the Randle cycle (which the study explicitly mentions). While the study did not look at what happened after the study ended, I'd venture a guess that the poor rodents subjected to pharmacologically increased FAO became insulin-resistant and gained even more weight than the control group after the torture ended. Hopefully, there will be a follow up study that will look at the long-term effects AFTER the stress signal (FAO) is no longer present, and what interventions could restore metabolism back to normal. The study did mention that the role of FAO in diabetes and obesity is "controversial" with some studies finding benefit while others finding FAO detrimental. The current study did NOT find any benefit of increased FAO for insulin sensitivity. So, until we see more follow up studies, the conclusion I'd draw from this study is that stress and its resulting increase in FAO ("endurance" exercise anyone?) is not only not a healthy way to lose weight, but for most people likely won't even work.

Acute or chronic upregulation of mitochondrial fatty acid oxidation has no net effect on whole-body energy expenditure or adiposity. - PubMed - NCBI

"...Body weight and fat mass in mammals are highly robust parameters. Fat mass is very well defended rendering many lifestyle interventions ineffective and so there is a growing need for new therapies. The hypothesis that manipulations which enhance fat burning will reduce adiposity has provided novel avenues and new hope for the treatment of obesity. Indeed there is a link between AMPK activation and leanness (Lage et al., 2008; Narkar et al., 2008). Currently the precise mechanism linking AMPK to leanness is unknown as AMPK activity has both short and long-term effects. On one hand AMPK rapidly increases FAO, primarily via its inhibition of ACC. On the other its prolonged activity regulates many other pathways such as mitochondrial biogenesis (Bergeron et al., 2001; Winder et al., 2000), uncoupling protein expression (Narkar et al., 2008; Suwa et al., 2003), GLUT4 expression (Winder et al., 2000), and the SIRT1 pathway (Canto et al., 2009). Hence, it is unclear if AMPK agonists promote leanness via the FAO pathway or an alternate route (Fig 4G)."

"...To address this question we used pharmacological and genetic manipulations in rodents to increase FAO upstream or downstream of AMPK. We used AICAR to activate AMPK acutely and chronically for 10 days. There was no change in body composition, substrate utilization, or energy expenditure following AICAR treatment at either time point, but there was a clear stimulation of mitochondrial biogenesis in skeletal muscle after 10 days. To test the effects of long-term changes in FAO independently of AMPK we directly targeted ACC2 in mice. ACC2 inhibition led to reduced intracellular malonyl-CoA levels and a concomitant increase in FAO in skeletal muscle without any change in energy expenditure or adiposity. Rather, in both acute and chronic settings, our data show that increased FAO is offset by an alteration in the handling of other macronutrients. Our findings are consistent with previous studies using a non-selective ACC1/2 inhibitor in rats. This inhibitor decreased RER over a 3 h period without altering energy expenditure (Harwood et al., 2003). Secondly, reduced ACC1/2 expression in rat liver and fat using antisense oligonucleotides was without effect on body weight (Savage et al., 2006). This illustrates that increased FAO is insufficient to promote energy expenditure or weight loss. Rather, the inherent flexibility in the metabolic system compensates for enforced FAO by altering carbohydrate metabolism. Such an effect is consistent with the glucose-FA cycle first proposed by Randle (Randle, 1963)."

"...Excess adiposity and lipid accumulation in non-adipose tissues are linked to insulin resistance (Savage et al., 2007). However the effect of increasing FAO on insulin sensitivity is controversial in that some studies indicate that enhancing FAO protects against HFD-induced insulin resistance (Bruce et al., 2009), while other studies show that excessive FAO in fact promotes insulin resistance (Koves et al., 2008). In our study we were unable to observe any protective effect of increased FAO against HFD-induced insulin resistance."

"...Based on the present study it is unlikely that increasing lipid oxidation alone is sufficient to cause leanness. In view of the fact that increased FAO was considered one of the major mechanisms of AMPK in fat reduction and leanness, this leaves open the possibility that the adipose lowering effects of chronic AMPK activation are mediated via an alternate pathway such as increased mitochondrial biogenesis or increased expression of uncoupling proteins."

Per Wikipedia "Fatty acids are preferentially oxidized because of the inactivation of PDH by fatty acid oxidation inhibiting glucose oxidation. This suggests that mitochondrial metabolism may control fuel selection. Cellular respiration is stimulated by fatty acids and this relates to an increase in the mitochondrial NADH to NAD+ ratio, suggesting that energy provision overtakes energy consumption. Switching from glucose to fatty acid oxidation leads to a bigger proportion of electrons being transported to complex 2 rather than complex 1 of the respiratory chain. This difference leads to a less efficient oxidative phosphorylation. By oxidizing fatty acids, mitochondria increase their respiration while increasing the production of ROS.[5] "

Great cancer scenario...Cancer will use the ROS for stress signaling...

 

[LucyL]

If you eat fat while you take Orlistat you will poop it out as an orange oil (sorry) Currently taking it with every meal but I am also trying to eat low fat so I don't have the orange mess. You can buy it at Walmart under the name Alli here in the US. Mildronate works by blocking Carnitine forcing the mitochondria to use Glucose instead of FAO. You can order it on Amazon Prime.

What is your primary source of calcium if you are trying to keep fat really low?

 

[Obi-wan]

What is your primary source of calcium if you are trying to keep fat really low?

Probably leaves in salads. I do eat some cheese

 

[haidut]

Most bodybuilders use caloric deficit, cardio, sometimes fasted, and then use stimulants like the ECA stack, etc. You never really know what those top guys are using, especially those that claim to be natty but most of them do it the stressful way and just use anabolic and thyroid hormones to try to negate the negatives.

@Steve

I would like to add to this that most bodybuilders use steroids and most anabolic steroids are glucocorticoid antagonists, hence their "anabolic" (really more anticatabolic/anticortisol) effect. Anything that blocks cortisol seems to prevent or largely limit fat gain, as well as allow the muscles to metabolize the excess fat. Trenbolone is notorious for allowing massive amount of calories to be eaten without much fat gain and is being tested as a potential treatment for obesity and metabolic syndrome striking so many middle-aged people. It just so happens that trenbolone has higher affinity for GR than even dexamethasone and is an antagonist at that receptor.
Structural Requirements For An Optimal Anti-Catabolic Steroid

Testosterone seems to be a double-edged sword likely due to its conversion to estrogen, but if it is combined with an AI it will probably function similar to trenbolone. Other non-aromatizable, potent anticatabolic steroids likely will have the same effects but there aren't many out there that are safe. HED of trenbolone in the studies below was 0.3mg/kg/day and duration of study was 4-6 weeks.

I think progesterone may also work in doses of 30mg-50mg daily if it is balanced by adding 5mg-10mg DHEA daily.

Trenbolone Improves Cardiometabolic Risk Factors and Myocardial Tolerance to Ischemia-Reperfusion in Male Rats With Testosterone-Deficient Metaboli... - PubMed - NCBI
"...The increasing prevalence of obesity adds another dimension to the pathophysiology of testosterone (TEST) deficiency (TD) and potentially impairs the therapeutic efficacy of classical TEST replacement therapy. We investigated the therapeutic effects of selective androgen receptor modulation with trenbolone (TREN) in a model of TD with the metabolic syndrome (MetS). Male Wistar rats (n=50) were fed either a control standard rat chow (CTRL) or a high-fat/high-sucrose (HF/HS) diet. After 8 weeks of feeding, rats underwent sham surgery or an orchiectomy (ORX). Alzet miniosmotic pumps containing either vehicle, 2-mg/kg·d TEST or 2-mg/kg·d TREN were implanted in HF/HS+ORX rats. Body composition, fat distribution, lipid profile, and insulin sensitivity were assessed. Infarct size was quantified to assess myocardial damage after in vivo ischaemia reperfusion, before cardiac and prostate histology was performed. The HF/HS+ORX animals had increased sc and visceral adiposity; circulating triglycerides, cholesterol, and insulin; and myocardial damage, with low circulating TEST compared with CTRLs. Both TEST and TREN protected HF/HS+ORX animals against sc fat accumulation, hypercholesterolaemia, and myocardial damage. However, only TREN protected against visceral fat accumulation, hypertriglyceridaemia, and hyperinsulinaemia and reduced myocardial damage relative to CTRLs. TEST caused widespread cardiac fibrosis and prostate hyperplasia, which were less pronounced with TREN. We propose that TEST replacement therapy may have contraindications for males with TD and obesity-related MetS. TREN treatment may be more effective in restoring androgen status and reducing cardiovascular risk in males with TD and MetS."

The effects of visceral obesity and androgens on bone: trenbolone protects against loss of femoral bone mineral density and structural strength in ... - PubMed - NCBI
"...RESULTS: Diet-induced visceral obesity resulted in decreased bone mineral area (BMA) and content (BMC) and impaired femoral stiffness and strength. Orchiectomy further impaired BMA, BMC and BMD and reduced energy to failure in viscerally obese animals. Both TEST and TREN treatment restored BMA, BMC, BMD and energy to failure. Only TREN reduced visceral adiposity and improved femoral stiffness and strength."