Hope it’s OK to promote myself, but I’ve made a few video’s about my PCOS journey and now I’m going to start including some videos about my Keto journey too!!
Here is a link to my Channel 
I'm sharing my PCOS and Keto journey on YouTube
Bethany
(Bethany Greenwood)
#3
Very interesting. Maybe the infertility rate of women with PCOS would be lower if we didn’t get the advice to “Go loose weight” ??
atomicspacebunny
(Bunny)
#4
This is fascinating stuff not just PCOS but obesity in general (sex hormone perspective), every time I see something unrelated the picture is becoming clearer to me:
image link
[1] “…Weight loss is often accompanied by resumption of ovulation in obese women with PCOS (33). The mech- anism underlying this response remains unclear. One consideration is that calorie restriction and/or the concomitant reduction of plasma insulin and/or leptin concentrations may be responsible. A negative energy bal- ance dampens pulsatile LH secretion in various mammalian species, including humans (for review see Ref. 55). Diminished central nervous system glucose oxidation appears to play a role in the regulation of LH secretion in response to calorie restriction in the rat and sheep. In addition, caloric deprivation is associated with a marked decline in leptin output, which in the rodent plays a critical role in reproductive physiology. Leptin relays nutritional status information to the hypothalamic GnRH neuronal ensemble, which controls gonadotropin secretion (for review see Ref. 8). Thus exogenous leptin administration partially rescues hypogonadotropism induced by starvation in female rats and male mice (1, 29). Concomitantly, the hyperinsulinism of PCOS may modulate LH secretion (15). Therefore, relative hypoinsulinemia induced by calorie restriction may provide an additional mechanism to suppress LH secretion in women with PCOS when undergoing weight loss. We hypothesized that short-term calorie restriction would repress inappropriate LH secretion in obese women with PCOS and ameliorate the hyperandro- genic milieu, possibly in association with attendant normalization of leptin and insulin secretion. To test this hypothesis, we measured 24-h plasma concentra- tions of LH, leptin, and insulin and ovarian steroids in the basal condition and after 7 days of a very low calorie diet (VLCD) in obese women with PCOS and compared the results with those in a group of body mass index (BMI)-matched women with regular menstrual cycles. …More
[2] Neurotensin makes us fat: “…In response to ingesting fat, enteroendocrine cells of the small intestine release the 13–amino acid peptide neurotensin (NT). Increased abundance of the NT precursor pro-NT in the circulation is associated with increased risk for developing diabetes and cardiovascular disease. Li et al . found that mice lacking NT or treated with an NT receptor antagonist stored less fat and absorbed less dietary fatty acids than wild-type (WT) littermates, even when fed a high-fat diet (HFD). NT–/– mice did not expend more energy or consume less food than WT mice, but they were protected from obesity, obesity-associated insulin resistance, and hepatic steatosis when fed a HFD. In cultured rat intestinal epithelial cells, NT stimulated fatty acid uptake, whereas knocking down NT receptors reduced fatty acid uptake. Activation of the metabolic regulator AMPK (adenosine 5′-monophosphate–activated protein kinase), which stimulates lipolysis and inhibits fat storage, was increased in the intestines of NT–/– mice fed a standard diet. In cultured rat and human intestinal cells, NT reduced AMPK activation in response to oleate and prevented a pharmacological activator of AMPK from reducing fatty acid absorption. Expressing human NT in the enteroendocrine cells of fruit flies reduced the activation of AMPK in the gut and increased the accumulation of lipid droplets in cells and tissues involved in lipid processing and energy storage. Feeding these flies a HFD further increased fat accumulation. The authors also found that obese and insulin-resistant people had increased plasma pro-NT and that high plasma pro-NT in nonobese people correlated with increased risk for developing obesity later in life. Thus, NT has an evolutionarily conserved function in stimulating fat absorption and plays a role in HFD-induced obesity. …”
[3] “…Neurotensin is a 13 amino acid neuropeptide that is implicated in the regulation of luteinizing hormone and prolactin release and has significant interaction with the dopaminergic system? …“ …More
[5] “…Luteinizing hormone (LH, also known as lutropin and sometimes lutrophin[1]) is a hormone produced by gonadotropic cells in the anterior pituitary gland. In females, an acute rise of LH (“LH surge”) triggers ovulation[2] and development of the corpus luteum. In males, where LH had also been called interstitial cell–stimulating hormone (ICSH),[3] it stimulates Leydig cell production of testosterone.[2] It acts synergistically with follicle-stimulating hormone (FSH). …” …More
Bethany
(Bethany Greenwood)
#6
Thank you very much!! it’ll be peppered with a few more Keto things now too 
timebuster
#7
I was particularly interested in your PCOS video.
I too have issues with high cortisol. One of the first measures I took to relieve my high cortisol was to switch over to decaffeinated coffee in the morning. I realize drinking caffeinated coffee especially first thing in the morning I became super anxious. I made it my business not to listen to the news instead of the first few hours in the morning I would listen to music from the 70s. Just changing those two bad habits has made a world of difference. I feel much calmer and relaxed to start my day.
Good luck with your upcoming videos.
Bethany
(Bethany Greenwood)
#9
Thank you!
Yes, I changed from coffee to green tea which felt better! I also do yoga now in the moring which really helps