https://www.sciencedirect.com/science/article/pii/S2666379121002664?fbclid=IwAR3uOYsNrPnl6nBeN8qFCDkytugK8YZQg7dPtn5sNgmuAaP4XUFKqe8cl9Q

A lot of talk about how positive thermogenesis is. But is it all positive?

Note that histamine reaction seem to cause thermogenesis and that isn't very positive. It will probably ruin your sleep which means bad news for your metabolism.

It's important that we not only get warmer but also feel better about it.

Perhaps I'm over-thinking this but I thought it was worth mentioning.

I recently read all of the u/fire_inabottle blogs about body fat PUFA causing low SDH activity, inducing topor, and the various methods that might break the topor cycle by increasing ROS production. I had already been investigating the benefits of LLLT (red light therapy) on the ATP process, particularly in how red light exposure generates ROS ([red light info here] (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2996814/)) and high ATP output. I know from my own experience that red light exposure results in higher energy levels. I'm curious if red light might be a way to generate thermogenesis and escape topor.

Since LLLT (low-level laser therapy aka red light therapy aka photobiomodulation) is poorly understood, I wanted to share some information about it and how it might be useful for healing our PUFA-damaged metabolisms.

LLLT is typically used in medicine for three main purposes: to promote wound healing, tissue repair, and the prevention of tissue death; to relieve inflammation and edema because of injuries or chronic diseases; and as an analgesic and a treatment for other neurological problems. Modern LLLT devices are LED-based and generally use a combination of infrared and near-infrared wavelengths (600–1070 nm).

My interest with LLLT started with sunbathing in the winter, trying to counter my seasonal depression. I found that morning sunlight made me feel better and more energetic than sunlight from later in the day, and research revealed that morning light has the more red light wavelengths. I bought an inexpensive red light device and started using it in the mornings, and found it gave me a strong boost. Researching the science of why it helped, I found out about LLLT.

The primary mechanism I’m interested in is how LLLT interacts with the mitochondria and ATP cycles. The simple version is here, and the complicated version below.

When red light wavelengths reach the mitochondria, there is a photochemical reaction. This happens in the electron transport chain at complex IV, also known as cytochrome c oxidase (CCO). The exact mechanisms are still being studied, but two significant things happen: one is that Nitric Oxide (NO) is released from the CCO, increasing NO in the bloodstream and lowering blood pressure, while also freeing up the CCO for oxygen; cellular respiration functioning is increased and more ATP is produced. The other result is that the successful creation of ATP released Reactive Oxygen Species (ROS). Red light produces a significant boost to ATP production, and therefore a significant amount of NO and ROS.

Reading through fireinabottles’s blog, with the ROS theory of obesity, the basic problem is that bodies with too much (poly)unsaturated fats become stuck in a low-ROS generating state. We need a way to switch our bodies back to a high-ROS generating state, with a healthy saturated fat-based feedback system. FIAB has been focused on enzyme management (targeting SCD1) through various supplements, but if the essential problem is the need for more ROS, LLLT may be able to provide that without risk of side effects.

https://fireinabot

Altered brown fat thermoregulation and enhanced cold-induced thermogenesis in young, healthy, winter-swimming men

• Susanna Søberg
• Johan Löfgren
• Frederik E. Philipsen
• Bente K. Pedersen
• Kristian Karstoft
• Camilla Scheele 7
• Show all authors
• Show footnotes

Open AccessPublished:October 11, 2021DOI:https://doi.org/10.1016/j.xcrm.2021.100408

Highlights

• Winter swimmers have a lower core temperature at a thermal comfort state than controls
• Winter swimmers had no BAT glucose uptake at a thermal comfort state
• Winter swimmers have higher cold-induced thermogenesis than control subjects
• Human supraclavicular skin temperature varies with a diurnal rhythm

Summary

The Scandinavian winter-swimming culture combines brief dips in cold water with hot sauna sessions, with conceivable effects on body temperature. We study thermogenic brown adipose tissue (BAT) in experienced winter-swimming men performing this activity 2–3 times per week. Our data suggest a lower thermal comfort state in the winter swimmers compared with controls, with a lower core temperature and absence of BAT activity. In response to cold, we observe greater increases in cold-induced thermogenesis and supraclavicular skin temperature in the winter swimmers, whereas BAT glucose uptake and muscle activity increase similarly to those of the controls. All subjects demonstrate nocturnal reduction in supraclavicular skin temperature, whereas a distinct peak occurs at 4:30–5:30 a.m. in the winter swimmers. Our data leverage understanding of BAT in adult human thermoregulation, suggest both heat and cold acclimation in winter swimmers, and propose winter swimming as a potential strategy for increasing energy expenditure.

Hi, new to this community.

I been reading and watchinf videos and I cant seem to find this soecific anawer.

So this is what ai understand (maybe you can correct me too). When you eat carbs, turns to glycogen, goes into blood stream and insulin comes in. Sugar is stored first into muscles, then Liver, ans rest as fat.

So, if all the carbs, plant based that is, I eat, is used up from moving/exercises/or sleeping(thermogenesis), then insulin takes sugar from muscles (assuming im eating proteins chickpeas too etc), it would be burned off first, then liver sugars is burned off.

So, if in eating alot of good carbs, how is my stored fat from many many years, will burn off if insulin keeps burning my sugars and not my fat ?

I can think of the laws of thermodynamics (thermogenesis) ,if im eating so much of the water density plant based carbs, im getting full so less calories and therefore, the rest would be my stored fat ? And if so, is that from walking, some exercise and fidgeting and sleeping all mixed together to burn it ?

Hope this makes sense 🙃

https://doi.org/10.1096/fj.202100298RR

https://pubmed.ncbi.nlm.nih.gov/34309918

Abstract

White adipose tissue (WAT) has the capacity to undergo a white-to-beige phenotypic switch, known as browning, in response to stimuli such as cold. However, the mechanism underlying beige adipocyte formation is largely unknown. Apolipoprotein E (ApoE) is highly induced in WAT and has been implicated in lipid metabolism. Here, we show that ApoE deficiency in mice increased oxygen consumption and thermogenesis and enhanced adipose browning pattern in inguinal WAT (iWAT), with associated characteristics such as increased Ucp1 and Pparγ expression. At the cellular level, ApoE deficient beige adipocytes had increased glucose uptake and higher mitochondrial respiration than wild-type cells. Mechanistically, we showed that ApoE deficient iWAT and primary adipose precursor cells activated the thermogenic genes program by stimulating the production of ketone body β-hydroxybutyrate (βHB), a novel adipose browning promoting factor. This was accompanied by increased expression of genes involved in ketogenesis and could be compromised by the treatment for ketogenesis inhibitors. Consistently, ApoE deficient mice show higher serum βHB level than wild-type mice in the fed state and during cold exposure. Our results further demonstrate that the increased βHB production in ApoE deficient adipose precursor cells could be attributed, at least in part, to enhanced Cd36 expression and CD36-mediated fatty acid utilization. Our findings uncover a previously uncharacterized role for ApoE in energy homeostasis via its cell-autonomous action in WAT.

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Open Access: False

Authors: Chung‐Lin Jiang - Ying‐Fang Chen - Fu‐Jung Lin -

Additional links: None found

Full-text: ncbi.nlm.nih.gov/pmc/articles/PMC5133058

The activity you do all day that isn't deliberate exercise nonexercise activity thermogenesis (NEAT). This activity includes walking, driving, gardening and even fidgeting. NEAT accounts for about 100-800 calories daily.

1. Introduction

> The meal consumed after an overnight fast, generally referred to as breakfast, is often described as ‘the most important meal of the day’ [1] as it is believed to contribute to good health and nutrition by providing essential nutrients early in the day [2]. Skipping breakfast is associated with increased weight gain and obesity, suggesting that breakfast may be protective against weight gain [1,3]. Among the explanations for this protective effect of breakfast are that it stimulates the body’s metabolism because it breaks the overnight fast [4], potentially contributing to increased total daily energy expenditure. The extent of this effect would depend on the diet induced thermogenesis (DIT) response to the meal consumed.
>
>[...]
>
> Obesity is a major public health concern internationally with an estimated 13% and 39% of adults worldwide being obese or overweight respectively [7], and 63% being either overweight or obese in Australia [8].

"Percent of adults aged 20 and over with overweight, including obesity: 73.6% (2017-2018)" cdc.gov/nchs/fastats/obesity-overweight.htm

2. Materials and Methods

> With the assistance of a research librarian, four databases were searched [...]

Cochrane, Cinahl, Embas, Medline

Randomized cross over designs with minimum of two meals

Hi. I did an elemental diet for eight days and gained a pound. I follow a macros program normally and eat specific grams of protein, carbs, and fat. The macros were the same (so calories were the same) for the elemental diet as my normal diet.

The only thing I could think of that would account for weight gain is decreased thermogenesis from not digesting food. I didn’t think about this ahead of time, but digestion, especially protein digestion, burns a fair amount of calories.

After the fact, this seems like a pretty obvious effect of an elemental diet. Now I’m really curious why I haven’t seen this mentioned anywhere.

Has anyone else had a similar experience?

Background

The question of whether there is daytime time variation in diet-induced thermogenesis (DIT) has not been clearly answered. Moreover, it is unclear whether a potential diurnal variation in DIT is preserved during hypocaloric nutrition.

Objective

We hypothesized that DIT varies depending on the time of day and explored whether this physiological regulation is preserved after low-calorie compared with high-calorie intake.

Design

Under blinded conditions, 16 normal-weight men twice underwent a 3-day in-laboratory, randomized, crossover study. Volunteers consumed a predetermined low-calorie breakfast (11% of individual daily kilocalorie requirement) and high-calorie dinner (69%) in one condition and vice versa in the other. DIT was measured by indirect calorimetry, parameters of glucose metabolism were determined, and hunger and appetite for sweets were rated on a scale.

Results

Identical calorie consumption led to a 2.5-times higher DIT increase in the morning than in the evening after high-calorie and low-calorie meals (P < .001). The food-induced increase of blood glucose and insulin concentrations was diminished after breakfast compared with dinner (P < .001). Low-calorie breakfast increased feelings of hunger (P < .001), specifically appetite for sweets (P = .007), in the course of the day.

Conclusions

DIT is clearly higher in the morning than in the evening, irrespective of the consumed calorie amount; that is, this physiological rhythmicity is preserved during hypocaloric nutrition. Extensive breakfasting should therefore be preferred over large dinner meals to prevent obesity and high blood glucose peaks even under conditions of a hypocaloric diet.

https://academic.oup.com/jcem/article/105/3/dgz311/5740411

https://doi.org/10.1038/s41467-020-20665-4

https://pubmed.ncbi.nlm.nih.gov/33436607

Abstract

Adipose tissue-resident T cells have been recognized as a critical regulator of thermogenesis and energy expenditure, yet the underlying mechanisms remain unclear. Here, we show that high-fat diet (HFD) feeding greatly suppresses the expression of disulfide-bond A oxidoreductase-like protein (DsbA-L), a mitochondria-localized chaperone protein, in adipose-resident T cells, which correlates with reduced T cell mitochondrial function. T cell-specific knockout of DsbA-L enhances diet-induced thermogenesis in brown adipose tissue (BAT) and protects mice from HFD-induced obesity, hepatosteatosis, and insulin resistance. Mechanistically, DsbA-L deficiency in T cells reduces IFN-γ production and activates protein kinase A by reducing phosphodiesterase-4D expression, leading to increased BAT thermogenesis. Taken together, our study uncovers a mechanism by which T cells communicate with brown adipocytes to regulate BAT thermogenesis and whole-body energy homeostasis. Our findings highlight a therapeutic potential of targeting T cells for the treatment of over nutrition-induced obesity and its associated metabolic diseases.

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Open Access: True

Authors: Haiyan Zhou - Xinyi Peng - Jie Hu - Liwen Wang - Hairong Luo - Junyan Zhang - Yacheng Zhang - Guobao Li - Yujiao Ji - Jingjing Zhang - Juli Bai - Meilian Liu - Zhiguang Zhou - Feng Liu -

Additional links:

https://www.nature.com/articles/s41467-020-20665-4.pdf

https://doi.org/10.1038/s41467-020-20665-4

https://doi.org/10.3390/metabo11020124

https://pubmed.ncbi.nlm.nih.gov/33671745

Abstract

Thermogenesis is an energy demanding process by which endotherms produce heat to maintain their body temperature in response to cold exposure. Mitochondria in the brown and beige adipocytes play a key role in thermogenesis, as the site for uncoupling protein 1 (UCP1), which allows for the diffusion of protons through the mitochondrial inner membrane to produce heat. To support this energy demanding process, the mitochondria in brown and beige adipocytes increase oxidation of glucose, amino acids, and lipids. This review article explores the various mitochondria-produced and processed lipids that regulate thermogenesis including cardiolipins, free fatty acids, and acylcarnitines. These lipids play a number of roles in thermogenic adipose tissue including structural support of UCP1, transcriptional regulation, fuel source, and activation of cell signaling cascades.

------------------------------------------ Info ------------------------------------------

Open Access: True

Authors: Helaina Von Bank - Mae Hurtado-Thiele - Nanami Oshimura - Judith Simcox -

Additional links:

https://www.mdpi.com/2218-1989/11/2/124/pdf

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7926967

I'm hoping that some of you very smart people can help me, because I am real confused here! There is so much information out there, and some of it appears to be very contradictory, so I'm not really sure what to do...

I want to strengthen my fasting practice to lose weight safely and effectively, without affecting my metabolic rate (adaptive thermogenesis), and also increase my time spent in autophagy for its myriad health benefits.

Dr. Jason Fung shows that ADF fasting doesn't significantly affect RMR, but I can't find much more information on the subject.

How many hours must one fast before their metabolism increases, and how much does it increase? I found one study which said fasting for 12 hours increased it slightly, but the effects were greatest at 36 hours. Does anyone have any additional information on this? Would eating OMAD (23 hour fast) increase your metabolism enough to offset the adaptive thermogenesis from eating less calories? Or would you need to do longer fasts (36 hours) a few times a week, or something along those lines? How long is your metabolism increased for?

Also, a lot of these studies mention that subjects are still eating during their fasting windows, such as advising people to consume 500 calories on their 'fasting days' while doing ADF. Wouldn't eating such a restricted amount of calories result in adaptive thermogenesis? Isn't this counter-intuitive? How many calories do you need to consume for it to be considered "low calorie" enough to trigger this? Where is the line between what the body considers a fast and very low calorie?

I also have to take medication every morning- is the amount of protein in the gelatin capsule enough to stop autophagy? If I continue to fast after taking the medication, will autophagy return quickly after the capsule has been digested? Or does the body have to start all over again?

Sorry this has turned into a wall of text...I just have so many questions! Also I'm just a lay person who doesn't fully understand all of the big sciencey words and jargon and methodology used in the studies. I just want to lose weight and get healthy and not completely bone my metabolism in the process!

I'm looking for the supplementary figures of this paper :)

https://www.sciencedirect.com/science/article/abs/pii/S1550413120300139?via%3Dihub#!

PMID: 32084379

DOI: https://doi.org/10.1016/j.cmet.2020.01.012

I have read many studies which are proved that protein consumption increases thermogenesis but exactly how ? any mechanism any theory any hypothesis ? please im dying to know