[Lotus]

Lotus,  My current weight is hoovering around 215, my goal is to be  under 180. I am doing a low carb diet with periodic fasting. I have to add more exercise than I am doing now, but my plans are to add primarily CardioVascular exercise like a treadmil with mimimal workouts with the weight machines. 

Ok, that's a doable goal. 

As for my diet, I am eating only one meal a day after 6:00 PM and no food after midnight. I do drink coffee and tea during the day.

MY medications are as follows Metformin 500mg, Fenofibrate 160mg, Atorvastatin 20 MG, Tamsolosin HCK .4 mg, Lorsartan Potassium 100 mg and Vitamin D3. I do have a regular family practice doctor, and no, I have not spoken to him about this. I think if I were going to talk to a doctor on this topic, I would want to find one to adress just this part of my care I can understand the need to keep some items like the liver in check. I have been told that I have fatty liver and my while my liver enzymes are in normal status and are checked annually they are not necessarily checked on each 4 month visit for my diabetes.

Please don't be offended by the attached study regarding diabetic obese men, I know your not obese. Where interested in what metformin does in diabetics. I was worried about you taking PM and SP (still am, lol) however if you only keep to 500 mg of PM (combined with the other meds) you should benefit because of the synergy between them. Keep in mind that PM has a uncanny way of adding weight. I made a post of how PM adds about 500-700 calories per day (I'll have to find it), so beware it may negatively go against weight loss, but hey everyone's different. As I've stated I'm not a fan of SP. And you may not need that fir the simple reason metformin inhibits Testosterone, plus I think it also feminizes too. 

The meds your taking are actually going to help benefit NBE for you rather than hurt it. Not only does Metformin help with diabetes, it also helps with anti-aging. Metformin is an AMPK activator (AMP-activated protein kinase), that is the mechanism for longevity. It also initiates ATP production (ATP-adenosine triphosphate). ATP is described as the energy currency for cells...meaning it has a lot to do the citric acid cycle, also known as the Krebs cycle. And ATP and cAMP (pro-aromatase) work together inside the mitochondria to make energy needed for cell growth (there's a more technical version to this action, lol). 

So basically AMP-activates protein kinase which  stimulates the breakdown of glucose for energy...which is ATP

And the Fenofibrate looks to be a fat/carb metabolizer. And in this respect it liberates fat cells which stimulate aromatase. 
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Research

The effects of metformin and diet on plasma testosterone and leptin levels in obese men
Abstract
Objective: The aim of this study was to investigate the effects of combined hypocaloric diet and metformin on circulating testosterone and leptin levels in obese men with or without type 2 diabetes.

Research methods and procedures: Twenty obese men with type 2 diabetes (mean body mass index [BMI]: 35.5 +/- 1.1 kg/m(2)) and 20 nondiabetic obese men were enrolled in the study. We measured serum follicle-stimulating hormone, luteinizing hormone (LH), total testosterone (TT), free testosterone (FT), sex-hormone-binding globulin (SHBG), dehydroepiandrosterone sulfate (DHEAS), and plasma leptin levels before and 3 months after metformin treatment. Both groups were placed on a hypocaloric diet and 850 mg of metformin taken orally twice daily for 3 months.

Results: Metformin and hypocaloric diets led to decreases in BMI and waist and hip circumferences in both groups. A significant decrease in TT levels in the diabetic group and FT levels in the control group was found, whereas follicle-stimulating hormone, LH, and DHEAS levels were not changed significantly. A significant increase in SHBG levels was observed in the control group but not in the patient group. Leptin levels also decreased after treatment in both groups. Decreased testosterone levels were not correlated to changes in waist and hip circumference, waist-to-hip ratio, BMI, and levels of fasting blood glucose, leptin, SHBG, or DHEAS in the diabetic group. However, a decrease in FT was correlated to changes in the levels of SHBG (r = -0.71, p = 0.001) and LH (r = 0.80, p = 0.001) but not to other parameters.

Discussion: We conclude that metformin treatment combined with a hypocaloric diet leads to reduced FT levels in obese nondiabetic men and to reduced TT levels in obese men with type 2 diabetes. Increased SHBG levels may account for the decrease in FT levels in the former group.
https://pubmed.ncbi.nlm.nih.gov/11707532

The Antidiabetic Drug Metformin Activates the AMP-Activated Protein Kinase Cascade via an Adenine 
Nucleotide-Independent Mechanism
Abstract

Metformin, a drug widely used to treat type 2 diabetes, was recently shown to activate the AMP-activated protein kinase (AMPK) in intact cells and in vivo. In this study we addressed the mechanism for this effect. In intact cells, metformin stimulated phosphorylation of the key regulatory site (Thr-172) on the catalytic (α) subunit of AMPK. It did not affect phosphorylation of this site by either of two upstream kinases in cell-free assays, although we were able to detect an increase in upstream kinase activity in extracts of metformin-treated cells. Metformin has been reported to be an inhibitor of complex 1 of the respiratory chain, but we present evidence that activation of AMPK in two different cell types is not a consequence of depletion of cellular energy charge via this mechanism. Whereas we have not established the definitive mechanism by which metformin activates AMPK, our results show that the mechanism is different from that of the existing AMPK-activating agent, 5-aminoimidazole-4-carboxamide (AICA) riboside. Metformin therefore represents a useful new tool to study the consequences of AMPK activation in intact cells and in vivo. Our results also show that AMPK can be activated by mechanisms other than changes in the cellular AMP-to-ATP ratio.


AMPK activators: mechanisms of action and physiological activities
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4855276/


The Antidiabetic Drug Metformin Activates the AMP-Activated Protein Kinase Cascade via an Adenine Nucleotide-Independent Mechanism
https://diabetes.diabetesjournals.org/content/51/8/2420
Studies in adipose tissue showed that treatment with ethynyl estradiol and progesterone, separately or in combination, increased lipoprotein lipase activity to a comparable extent. After treatment with progesterone alone, the increase was observed in the absence of elevated levels of triglycerides in blood. Triacylglycerol lipase activity assayed at pH 7.4 (hormone- sensitive lipase) was not affected by ethynyl estradiol or progesterone alone, but a significant decrease was observed under a combined regimen. None of these hormonal treatments modified the level of monoester lipase activity. Taken together, the results point to major hormonal influences on lipid metabolism in liver and adipose tissue. However, it cannot be assessed whether these effects are due to the direct action of ethynyl estradiol and progesterone on liver and adipose tissue lipases and/or to some other altered metabolic response (s) secondary to the intake of the steroids.
- See more at: http://press.endocrine.org/doi/abs/10.12...QzX1p.dpuf