Tools to reduce pro-inflammatory fat

There are 3 different types of fat or adipose tissue: WAT (white adipose tissue), BAT (brown adipose tissue) and beige.
White adipose tissue (WAT) is not only an energy reservoir but, being a highly active endocrine organ, it is closely related to obesity, increased pro-inflammatory cytokines, altered lipid profiles, blood glucose levels and subsequent insulin resistance.
Brown adipose tissue (BAT), on the other hand, is considered to be the body’s natural “heater” since, despite being one of the smallest fat deposits in humans, it converts chemical energy into heat.

KEY:
BW: body weight
FFM: fat free mass
FM: fat mass
Le: essential lipids (good)
BAT: thermogenic brown fat (good)
AAT: visceral or abdominal fat (bad)
IMAT: fat infiltrated between muscles, including heart (bad)
SAT: subcutaneous or superficial fat (good)
WAT: pro-inflammatory white fat (bad)
Beige: thermogenic and anti-inflammatory fat (good)
Browning: all activities leading to the loss and conversion of bad pro-inflammatory fat into good fat

Indeed, its effect is opposite to that of white adipose tissue. Brown fat is able to generate large amounts of heat thanks to the presence of UCP1 proteins on the inner mitochondrial membrane. When stimulated, UCP1s allow protons to flow freely through the mitochondria, bypassing the normal ATP production which occurs in the mitochondria of all other organs. At maximum stimulation, brown fat has the ability to generate up to 300 times more heat per unit mass than any other organ in the body and, as such, can account for up to 10% of total daily heat production. [1-6]
Another important difference between brown adipose tissue and white adipose tissue is innervation. Brown adipose tissue is highly innervated by the sympathetic nervous system (see measurement with PPG - Stress Flow device) compared to white adipose tissue, which is why brown adipose tissue is called “neuroendocrine thermogenic organ”. With age, brown adipose tissue is lost and/or replaced by white adipose tissue, but it contains small deposits of adipocytes called beige, that can be reactivated through the so-called “Browning” mechanism.
There are several methods investigated in literature to maximize the Browning effect with the aim of keeping the total amount of fat, especially white adipose tissue, at a low level and stimulate brown adipose tissue, so that it is not lost over the years.
Among these, there are high intensity and short duration workout (HIIT - high intensity interval training), cold stimulation and the restoration of nitric oxide bioavailability levels (bioavailability that is lost with the increase of white adipose tissue). [7]
The stimulation of the sympathetic nervous system through cold, if carried out in the morning when waking up (ideal time of the day), has proven to be an excellent method to adequately trigger brown adipose tissue. Additionally, this method also allows to prepare the body for the HIIT workout. As a matter of fact, it is important not to perform HIIT workout under parasympathetic dominance (see PPG - Stress Flow device), a very frequent condition in patients with MUS, affected by metabolic disorders and/or diseases resulting from the accumulation of white adipose tissue.
Finally, L-Arginine is an important precursor of nitric oxide. Physiological levels of L-Arginine modulate the key genes that are responsible for the expression of fatty acid and glucose oxidation, thus reducing white adipose tissue throughout the body. These changes are associated with lower circulating glucose and homocysteine levels (risk factors for metabolic syndrome) and improved endothelial-dependent relaxation (by nitric oxide) in both type I and type II diabetes mellitus. [8-12]

The use of negative PRAL L-Arginine dietary supplements with potassium and magnesium supplementation (e.g. Melcalin Pralginina), associated with Browning maximization methods, can be a crucial strategy for the prevention of and recovery from obesity, cardiovascular events and metabolic syndrome. The choice of a negative PRAL formulation finds ample room due to the buffer action of the minerals contained in it. Attention to the acid-base balance is key, especially in these conditions associated with the increase of white adipose tissue, such as dyslipidemia, increased abdominal circumference, insulin resistance, inflammatory and cardiovascular diseases. [13]

"Browning effect" sequence

The methods to maximize white adipose tissue oxidation (fat loss) and brown adipose tissue stimulation can be included in a simple but effective sequence to be performed before breakfast (to prolong the effect of glucagon):

  1. SCold stimulation in the region of greatest BAT concentration by placing gel ice packs in the sub-clavicular areas; as an alternative, the body can be exposed for a few minutes to the cold, for example, with a cold shower or by wiping wrists and face with cold water
  2. Respiratory biofeedback (see PPG - Stress Flow device): 5 seconds breathe in, 2 seconds hold, 5 seconds breathe out for at least 5 minutes. Ideally with PPG Stress Flow device to better control respiratory and heart rate variability
  3. Taking Melcalin Pralginina
  4. HIIT workout (ideally in an unheated environment): e.g. 20 minutes, alternating one minute of high intensity, one minute of pause for 10 times depending on one’s personal motor skills.

Authors: M. Lucafò, D. Boschiero - Date: 06/11/2020


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References

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  8. Pubchem. Compound Summary for CID 6322.
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  10. Jobgen W, Fu WJ, Gao H, Li P, Meininger CJ, Smith SB, Spencer TE, Wu G. High fat feeding and dietary L-arginine supplementation differentially regulate gene expression in rat white adipose tissue.Amino Acids 37(1) : 187-98. 2009
  11. Fu WJ, Haynes TE, Kohli R, Hu J, Shi W, Spencer TE, Carroll RJ, Meininger CJ, Wu GY. Dietary L-arginine supplementation reduces fat mass in Zucker diabetic fatty rats. J Nutr.135(4): 714-21. 2005
  12. Lucotti P. Et al. Beneficial effects of a long-term oral L-arginine treatment added to a hypocaloric diet and exercise training program in obese, insulin-resistant type 2 diabetic patients.Am J Physiol Endocrinol Metab. 291(5): E906-12. 2006
  13. Murakami K. et al. Association between dietary acid-base load and cardiometabolic risk factors in young Japanese women. Br J Nutr. 100 (3): 642-51. 2008