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PCOS Diet – How sugar affects insulin resistance & weight loss

By 14th Jul 2020Sep 3rd, 2022Lifestyle

Diet & PCOS

Diet is a very important lifestyle consideration for PCOS treatment in South Africa. In this article, we will unpack the affect that dietary sugar has on PCOS, as well as the best ways to counter this. It is also important to mention just how bad consuming sugar and sugar-containing foods (and drinks) maybe to potentially worsening PCOS symptoms and insulin resistance. It is commonly documented that women with PCOS will crave sugar and fried foods, which makes abstinence all the more challenging.


The inositols play an essential role in insulin signalling and the resultant removal of glucose from the blood stream into fat cells, muscle cells and liver cells.

When blood sugar levels are raised (hyperglycemia), glucose inhibits the intestinal absorption of inositol, increases renal excretion and reduces renal reabsorption resulting in overall loss in inositol.

In insulin resistance there is

  • decreased availability of inositols or inositol phosphoglycans (IPGs).
  • increased urinary loss of Myo-Inositol (MI) also known as Inositol Phosphoglycan –A [IPG-A]), resulting in reduced D-Chiro-Inositol (DCI which is Inositol Phosphoglycan-P [IPG-P]).

Plasma and intracellular depletion of MI/DCI or IPG metabolites is likely to worsen insulin resistance.

PCOS Diet, Inositols & Weight loss

From a dietary perspective, failure to stop sugar and sugar containing foods as well as eating high carbohydrate foods will likely exacerbate the lowering of overall Inositol phosphoglycans. This worsens physiological insulin signaling, resulting in insulin receptor resistance, raised blood insulin and raised blood glucose (as the very mechanism to remove glucose [insulin receptor and downstream signaling substrate molecules]), are now faulty. This, in a nutshell, will likely lead to weight gain and the inability to lose weight.

So how about Ketogenic diets with PCOS?

Where ketogenic /Banting style of carbohydrate avoidance is a method of glucose restriction and loss of fat mass and weight, there is a caveat with regard to the inositols. The main dietary source of inositols is cereals and grains.

Cereals and grains are a rich source of phytates/phytic acid which contain MI and also PI (phosphatidyl inositol and IP6 [Inositol 6 phosphate]). Eliminating all cereals and grains maybe disadvantageous with regard to dietary presence of inositols. Make sure to avoid processed cereals and grain products and opt for unprocessed grains and cereals in small amounts, as strict carbohydrate avoidance diet will likely be deficient in inositols.

Our bodies make this stuff too

The human body is not solely dependent of dietary inositols and can manufacture inositols endogenously (on it’s own). A metabolite of glucose, glucose-6-phosphate is the starting point of inositol production as myo-inositol. However high glucose levels will increase Phospholipase D (PLD), a key enzyme for PA (phosphatidic acid) which increases nuclear IP6K1 (Inositol hexakisphosphate kinase-1) which decreases MI content.

So to sum it up… Stay off the sugar for good amounts of naturally produced inositol

Over-activation of IP6K1 by insulin stimulation, promotes IP-7 (inositol pyrophosphates) which inhibits Akt  (protein kinase B) by preventing interaction with PI3K. Inhibited Akt reduces insulin sensitivity and protein synthesis. Insulin resistance increases GSK-3 (glycogen synthase kinase 3) and mTOR (mammalian target of Rapamycin) and associated with weight gain.

Hence a high sugar diet will not only reduce exogenous Inositol (inositol supplement) intake and retention, but will also compromise endogenous production (body’s production) of Myo-Inositol.

High blood pressure, metabolic syndrome, insulin resistance and the inositols

Since high blood sugar levels evoke higher and sustained insulin release, high insulin in the presence of insulin receptor resistance will suppress conversion of MI to DCI by suppressing epimerase. Low DCI will allow insulin resistance to continue unchecked which then worsens PCOS symptoms as Metabolic Syndrome develops (high glucose, high insulin, high blood pressure, high blood fats [triglycerides], high cholesterol and increased weight [increased fat mass]). Bringing DCI back into the insulin signalling mechanism is essential to reduce insulin receptor resistance, lower blood insulin levels, help weight loss and start the recovery process.

Both IPGs (MI/DCI) work as second messengers downstream of insulin receptors.

  • Upon Insulin receptor activation MI/DCI are transported into the cell, enhancing glucose breakdown and enhancing Kreb cycle activity as well as glycogen synthesis through the  
  • PI3K and Akt pathways which block glycogen breakdown (by inhibiting GSK-3) while increasing GLUT-4 translocation and glucose uptake. 
  • IPG-P (DCI) inhibits glucose stimulated release of insulin from pancreatic cells, suggesting a negative feedback and both MI and DCI have an anti-diabetic actions.  MI converts to DCI by epimerase which requires insulin.  Insulin resistance occurs in muscle, fat and liver insulin receptors where epimerization severely impaired and reduced DCI/MI ratio represents the degree of insulin resistance. The lower the DCI, the worse the insulin resistance.

Low DCI is typical in urine of type 2 diabetes (T2D) patients. In PCOS there may be a deficiency of membrane bound IPG phospholipids and or a reduction of epimerase dependent conversion of MI to DCI. This compounds insulin resistance and the Metabolic Syndrome.

PCOS, Insulin and the ovaries

What is the ‘DCI paradox’ ?

While there is a deficiency of DCI in tissues displaying insulin resistance (muscle, fat and liver), the ovaries remain insulin receptor sensitive and display increase DCI and reduced MI due to high insulin driving epimerization of MI to DCI. The impairment of ovarian function is associated with an increase in DCI/MI in the ovary.

To neutralise the DCI paradox, the aim is to lower insulin levels and by lowering insulin levels reduce the hyper-stimulation of insulin on the ovaries. This then likely reduces over production of DCI at an ovarian level.

DCI is critical for insulin homeostasis, so where low levels of DCI is necessary in the ovaries, higher levels are required at fat, muscle and liver insulin receptor signaling to reduce the Metabolic Syndrome and insulin resistance. 

Not everyone with PCOS benefits from synthetic MI/DCI supplements possibly due to the fact that natural IPG have additional critical co-factors, hence it is essential to enhance endogenous MI production and facilitate MI absorption through dietary intake, by lowering blood glucose and eating inositol rich phytates in grains and cereals.

When MI is taken up by a cell, it transforms into phosphatoinositides (PI3K) and phospholipids. PI3K is essential for downstream insulin signalling to activate the GLUT-4 transporter to migrate to the cell surface and literally open the ‘gate’ for glucose to enter the cell. Pi3K also facilitates glycogen synthesis (a storage form of glucose).

Inositols reduce glycemia and insulin resistance while buffering negative effects of insulin stimulation on adipose tissue and the endocrine system. Myo-inositol is being shown through multiple studies MI to improve insulin resistance in PCOS patients.

There have been a rash of studies testing the best ratio of MI/DCI.  Initially MI was found to improve ovarian function in 2gram daily doses. When small amounts of DCI were added in  varying amounts, less MI could be used to achieve similar results. Studies using 550mg MI  and 13mg DCI were found equivalent to  2g MI. However, other studies have reported enhanced ovarian function using high dose DCI 400mg (in spite of a known DCI excess at the ovaries in PCOS) and yet improvements were recorded. 

What About the 40:1 GOLDEN ratio

Until such time as the multiple layers of biological terrain is understood and seemingly infinite factors influencing insulin resistance and ovarian function are understood, the 40:1 of MI/DCI ratio is an approximation at best. However, severe insulin resistance is in part driven by the absence of DCI, and robust DCI supplementation can support insulin sensitivity which then changes the ‘state of play’ at the ovaries. 

LIFE SOURCE PCOS Support Supplement and the inositols

Until such time as insulin resistance is resolved, an improvement in PCOS is unlikely to occur. PCOS SUPPORT Supplement has a comprehensive insulin sensitising group of ingredients in the Metabolic Balance which support multiple aspects of the insulin signalling cascade from the insulin receptor through to the GLUT-4 transporter, blocking factors which down grade insulin signalling, while promoting insulin signal transduction, for the lowering of glucose levels and the lowering of insulin secretion.

Even the Hormone Balance bottle in the PCOS SUPPORT creation supports insulin sensitivity through Curcumin which attenuates the Metabolic Syndrome, lowering blood fats, lowering blood pressure, lowering LDL cholesterol, raising HDL cholesterol, blocking fat deposition, supporting fat burning and improving insulin sensitivity.

PCOS SUPPORT powerfully addresses a multitude of dysfunctional events in PCOS, by supporting the lowering of inflammation, the lowering of oxidative stress, the lowering of insulin resistance, the improving of ovarian function, the reducing of androgen excess and oestrogen excess and supporting progesterone.

PCOS Support and Pregnancy

South African women with severe PCOS who have used the standard of care and failed, including third tier treatments (surgical ovarian drilling and or IVF or similar procedures), have simply fallen pregnant after a few months of PCOS SUPPORT.

Natural supplementation is a very effective way to return the body to a harmonious state – in short, PCOS Support works, and helps women reduce PCOS symptoms, fall pregnant and lose weight.

Dr.R. Cooper is a South African PCOS specialist based Australia.

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