Our fat is so much more than a storage tissue for energy – it’s actually an endocrine organ – one that sends strong signals to our brains and hormonal systems. We used to think of fat as being quite inert, but evidence now shows that this couldn’t be further from the truth. Fat cells secrete signals that can alter the way our body functions.
As women, we all need body fat to maintain health, hormonal regulation and reproduction. When energy is stored in fat, the cells send out chemical messengers indicating that we have enough food in our environment to sustain us. Our brain engages in direct communication with our fat cells, learning from their signals when we have enough to eat – and when we need to eat more.
After we eat a meal, our fat cells secrete a hormone known as leptin – leptin travels up to the brain, messaging that we have enough stored energy and can stop intaking food. When we secrete leptin after fat is stored in the post-meal state – the brain quiets its appetite centre, turning off feelings of hunger. Leptin does more than regulate hunger, it also activates the reproductive pathways in the brain. In some cases, our brains can become resistant to the fullness signals of leptin, especially if there is an excess accumulation of fat – disrupting our natural signals of hunger and satiety.
Now, with that in mind, I’d like to introduce you to a term that is very important when it comes to understanding PCOS and it’s deepest root cause – this term is lipotoxicity.
Lipotoxicity means literally “fat-toxicity”. When fat cells become overly full, they start to leak their contents out into the blood, including fatty acids, leptin and other chemical messengers. When NEFAS (Non esterified Fatty Acids) leak from fat cells, they cause inflammation of massive proportion, also known as lipotoxicity. This inflammation causes problems with the way that our cells respond to insulin- and makes them insulin resistant. Yes that’s right – lipotoxicity is a major underlying cause of insulin resistance – and now is thought to be THE cause of insulin resistance in women with PCOS.
Think of it this way also – fat does not have good blood supply – it has very few arteries and veins compared to other tissues in the body. Deep inside the fat layers, the cells receive such poor circulation that they undergo something called fat necrosis (cell death). The fat cells begin to die – causing even more NEFAs to spill out which equals more inflammation.
So how does this relate to PCOS? Well, PCOS has recently been linked to basic differences in how our fat cells function.
It turns out that the fat cells of women with PCOS secrete higher levels of Non Esterified fatty acids (NEFAs) and inflammatory chemicals compared to women without PCOS, even when matched for body weight. It’s now thought that this is actually why women with PCOS have insulin resistance.
It’s now also known that lipotoxicity can contribute to the high androgen levels found in PCOS. Preliminary studies suggest that exposure to NEFAs increase testosterone output by the ovaries.
So how does all of this inflammation create havoc in the body? Inflammation is characterized activation of the immune cells – once activated, the cells secrete chemical messengers known as cytokines. Normally, in processes of infection – these cytokines activate other immune cells to kill off invaders like bacteria or viruses.
Our immune cells perform their attacks on viruses and bacteria by releasing hydrogen peroxide and other damaging chemicals. In chronic inflammation and lipotoxicity – as is found in PCOS – the immune system never turns off its attack mode – damaging many of our own cells in the body. Lipotoxocity causes the cell damage found in women with PCOS who have fatty liver, or pancreatic dysfunction, and as is most commonly seen in women of reproductive age, it profoundly impacts our ovaries as well.
Inflammation affects egg quality and disrupts ovulation by impairing the ability of the follicles to develop normally.
Part of the solution to the damaging effect of lipotoxity is in finding ways to help our bodies dispose of these excessive free fatty acids. Many of these pathways depend on antioxidants, like glutathione,
to quench the damaging chemicals generated as our bodies try to get rid of of the excess fatty acids. If our disposal pathways are strong, we can deal more effectively with lipotoxicity and get to the deepest, underlying causes of insulin resistance.
Diet can also impact lipotoxicity greatly – whole, healthful foods, rich in natural antioxidants are the key – and making permanent, sustainable changes to the diet rather than following a temporary “diet” is important, as PCOS is a lifelong condition.
A diet that minimizes inflammation and cell damage includes plentiful amounts of green and brightly coloured vegetables, lean proteins such as fish, small amounts of carbohydrate such as sweet potato or squash, small amounts of fruit, particularly berries – and healthy fats such as coconut oil and ghee (for hot use) or avocado oil and extra virgin olive oil (for cold use). These dietary changes can help our fat cells to perform more effectively in the face of inflammation.
It’s also important to avoid poor quality vegetable oils such as canola oil, soybean oil and corn oil, particularly if heated to high temperatures – these are basically like introducing NEFAs directly into the blood stream. These poor quality oils are structurally damaged and full of free radicals – creating more inflammation.
How are you reducing inflammation and improving cell health in your body – please share your ideas below!
- Celik O, Aydin S, Celik N, Yilmaz M. Peptides: Basic determinants of reproductive functions. Peptides. 2015 Jun 12.
- Bellanger S, Battista MC, Fink GD, Baillargeon JP. Saturated fatty acid exposure induces androgen overproduction in bovine adrenal cells. Steroids. 2012 Mar 10;77(4):347-53.
- Mannerås-Holm L, Leonhardt H, Kullberg J, Jennische E, Odén A, Holm G,Hellström M, Lönn L, Olivecrona G, Stener-Victorin E, Lönn M. Adipose tissue has aberrant morphology and function in PCOS: enlarged adipocytes and low serum adiponectin, but not circulating sex steroids, are strongly associated with insulin resistance. J Clin Endocrinol Metab. 2011 Feb;96(2):E304-11.
- Yu C. et al. Mechanism by which fatty acids inhibit insulin activation of insulin receptor substrate-1 associated phosphatidylinositol 3-kinase activity in muscle. J Biol Chem. 2002;277(52):50230-6
- Azziz et al. Troglitazone improves ovulation and hirsutism in the polycystic ovary syndrome: a multicenter, double blind, placebo-controlled trial. J Clin Endocrinol Metab. 2001;86(4):1626-32
- Carpentier AC. Postprandial fatty acid metabolisn in the development of lipotoxocity and type 2 diabetes. Diabetes Metab. 2008;34(2):97-107.
- Holte J et al. Serum lipoprotein lipid profile in women with the polycystic ovary syndrome: relation to anthropometic, endocrine and metabolic variables. Clin Endocrinol (Oxf). 1994;41(4): 463-71
- Mai et al. Free fatty acids increase androgen precursors in vivo. J Clin Endocrinol Metab. 2006;91(4):1501-7.
- Mai et al. Intravenous lipid and heparin infusion induced elevation in free fatty acids and triglycerides modifies circulating androgen levels in women: a randomized, controlled trial. J Clin Endocrinol Metab. 2008;93(10):3900-6.