The FastDay Forum

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I have been investigating the research into the variation in energy expenditure, thyroid function, leptin etc between people which might point to sources of variation in weight and weight loss and found a few interesting titbits:

The DLW [doubly labelled water] method has also been used to demonstrate that the interindividual differences in energy expenditure associated with physical activity are larger than those for RMR or the thermic effect of meals (TEM) and thus more likely to lead to major deficits or surfeits in energy balance.

Basically, some of us are more efficient in moving than others and this causes most of the variation in TDEE. (From

Twenty men and 34 women (20-36 years of age) provided complete anthropometric, accelerometer, resting metabolic rate (RMR), and DLW data. TEE and PAEE were determined for the same week that accelerometers were worn during waking hours. Accelerometer data included mean steps per day, peak 30-min cadence (average steps per minute for the highest 30 min of the day), and time spent in each incremental cadence band: 0 (nonmovement), 1-19 (incidental movement), 20-39 (sporadic movement), 40-59 (purposeful steps), 60-79 (slow walking), 80-99 (medium walking), 100-119 (brisk walking), and 120+ steps·min(-1) (indicative of all faster ambulatory activities). Regression analyses were employed to develop sex-specific equations for predicting TEE and PAEE. The final model predicting TEE included body weight, steps per day, and time in incremental cadence bands and explained 79% (men) and 65% (women) of the variability. The final model predicting PAEE included peak 30-min cadence, steps per day, and time in cadence bands and explained 76% (men) and 46% (women) of the variability. Time in cadence bands alone explained 39%-73% of the variability in TEE and 30%-63% of the variability in PAEE. Prediction models were stronger for men than for women.

Differences in the amount of walking around only accounted for around half of the variation in physical activity energy expenditure (PAEE) seen in women (from

BMI was positively associated with (F)T(3) (P<0.0001). Whole body fat mass displayed positive associations with TT(3) and with (F)T(4) and TBG (P≤0.0006). Positive associations were further observed between leptin and (F)T(3), TT(4), and TBG (P≤0.0002). Inverse associations between lean mass and muscle cross-sectional area and (F)T(3), (F)T(4), and TBG were observed (P≤0.0003). Higher levels of (F)T(3) and TBG were associated with lower insulin sensitivity, assessed by homeostatic model assessment of insulin resistance (IR; P≤0.0001). No associations between TSH and body composition or metabolic parameters were seen.

We show that a less favorable body composition (with higher fat and lower muscle mass and accompanying higher leptin concentrations) and IR are associated with higher thyroid hormone levels in healthy young men with well characterized euthyroidism.

Men with apparently normal thyroid function showed differences in body weight, fat mass and the appetite controlling hormone, leptin, that could be accounted for by differences in thyroid hormone levels (from

However, by contrast in a study aiming to determine predictors of weight loss in obese men participating in a 2-year behaviour modification programme:
At baseline, there were significant correlations between plasma leptin and body mass index (BMI), fat-free mass (FFM) and insulin resistance. Median weight loss over 2 years was 4.9 kg (range, -27.2 to +11.9). Baseline serum leptin concentrations adjusted for BMI (leptin/BMI ratio) were significantly correlated with 2-year weight change (r = 0.34, P = 0.04). A subset of seven of the 44 men gained weight over the 2 years. These 'gainers' differed significantly in initial leptin/BMI ratio (0.62 +/- 0.07) compared with the 37 'losers' (0.42 +/- 0.03, P < 0.05). In a multiple regression model, baseline leptin, insulin and age predicted 22% of the variance in weight change with no additional significant contribution from BMI, FFM, waist:hip ratio, thyroid function tests or energy intake. There was a strong correlation between the change in leptin concentrations and the change in insulin resistance from baseline to 2-year follow-up (r = 0.54; P < 0.001).

Baseline plasma leptin concentrations predicted long-term weight loss. Inappropriate leptin secretion or disposal, corrected for BMI, was associated with failure to maintain weight loss in obese men in a behaviour modification weight loss programme.

So in this group, leptin was the baddy not thyroid hormone (from

Lastly we have the conclusions of this interesting study on habitual dieters:
The results of the present study indicated differences in metabolic variables between the 2 groups of female chronic dieters; body-composition variables, particularly LBM, best predicted REE. The results also indicated that a normal REE was associated with insulin resistance. Insulin resistance has been shown to correlate positively with a high ratio of abdominal to gluteal fat mass, which was shown in women in the NREE group. Differences in leptin were likely due to normal diurnal variations rather than to the influence of food consumption or REE. The higher T4 and rT3 values in the NREE group support the positive association between thyroid production and metabolic rate; however, this difference has been shown mainly under conditions of energy restriction, which was not the case for the NREE group. More research is required to elucidate the complex interactions of insulin, leptin, and thyroid hormones in energy metabolism. The LREE group had higher dietary restraint than did the NREE group. This may partly explain the lower REE of the LREE group because dietary restraint has been shown to the reduce metabolic rate.

The female chronic dieters in the LREE group in the present study had a low LBM, low metabolic hormone concentrations, and high dietary restraint. Health promotion programs that emphasize regular physical activity and normalized eating behaviors (ie, a healthy diet) may be beneficial for this group.

Acronyms, doncha love em. I'm guessing:

REE = really eating everything
NREE = no rational explanation - ever
LBM = lesbian bisexual male

Don't tell me I got them all right...
It would be good if some obesity researchers looked hard at stalling / plateaus. It appears that anyone who exhibits a failure to lose weight is kicked off clinical trials for non-compliance, as far as I can see.

One guy wrote "the law of conservation of energy is universally valid apart from free living humans, primarily women, and possibly their pets".

The literature survey points to reductions in energy expenditure other than in the resting metabolism, which I can relate to. If you're hungry you may be less motivated to run around. On the other hand if I eat a lot I tend to fall asleep afterwards which will give a bigger deficit unlike falling asleep after 2 hours digging in the garden where the sleep cancels out the "exercise".
dominic wrote: Acronyms, doncha love em. I'm guessing:

REE = really eating everything
NREE = no rational explanation - ever
LBM = lesbian bisexual male

Don't tell me I got them all right...

Ha ha! :lol:
You forgot LREE = loving really eating everything

On a more serious note, it is interesting that the last paper identified a group of women with a low REE (resting energy expenditure) separate from the normal (NREE) group among this population of chronic dieters. They assume the LREE group have a low REE because of the dieting rather than they have to diet because of a low REE! Their findings are perhaps unsurprising though: subclinical thyroid dysfunction and low lean body mass (LBM) predict LREE. I think the dietary restraint element is likely to be a result rather than a cause of LREE. However, the LBM could be worth adding to the questionnaire...i.e. are participants mesomorph, ectomorph or endomorph (obviously phrased differently).

Re the leptin thing...anyone got any thoughts on the so called leptin reset protocol that I've seen mentioned on the web?
Re the leptin thing...anyone got any thoughts on the so called leptin reset protocol that I've seen mentioned on the web? and the like ? My normal response would be "Show me a clinical trial with leptin measurements and leptin resistance assessment".

4-6 weeks on a different diet will do something I guess, but whether it cures leptin resistance or whatever I have no idea.

I confess my "cause and effect" understanding of leptin is limited.... fat tissue produces leptin so fat people have high levels of leptin and the systems that respond to this become resistant or defective. Going on a diet reduces leptin levels but that probably doesn't matter in leptin resistant people as they're ignoring the messages anyway.

Jack Kruse's FAQ says

Can I skip lunch during the LR Protocol if I’m not hungry? Yes, it is good if you can make it until dinner without being hungry. Then, you can eat more at dinner if need be.

Can you do IF (Intermittent Fasting) in conjunction with the LR Protocol? No way. I love IFing, but don’t try it until you are leptin sensitive again. IFing requires the AMPk pathways to be working optimally.

He also says "Will the Leptin Reset fix insulin resistance? It is designed to eradicate it completely, if you do it correctly." - in which case a HOMA assessment would provide a measure of its effectiveness
What do you all think about Dr Rosedale's diet ideas? Seem hard to live up to in normal life to me.
Azureblue wrote: What do you all think about Dr Rosedale's diet ideas? Seem hard to live up to in normal life to me.

I could do it, the moderate protein is one I have to work at but less than 100g of carbs is a breeze.
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