Here is the second instalment from my partner to provide a female perspective and experience of LCHF diets.
Included are some references and recommended reading.

In my previous guest blog post, I alluded to a self-conducted experiment which involved the adoption of a low carbohydrate, high-fat diet (Fat, cholesterol and individuality – Part 1). In this I discussed the specifics of two completely different outcomes experienced by Jarrod (my partner) and me.

So, while I promised a research-based guide as to why I experienced a paradoxical rise in cholesterol, the research is well – sparse and inconclusive; however I shall do my best to explain!

As I discussed in Part 1, generally speaking, a low carbohydrate, high fat diet can decrease certain risk factors for lifestyle disease such as diabetes, obesity and cardiovascular disease. However some individuals see negative effects, including increases in cholesterol – particularly LDL cholesterol, lethargy and fatigue and weight gain.

As most of you will be aware, there are two main types of cholesterol – high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C). The latter is generally termed “bad” cholesterol as it is closely involved in the development of atherosclerosis, whereas HDL-C is generally accepted as the “good” cholesterol, having protective effects on the circulatory system and heart. However, what most people are not aware of (as this is rarely requested on blood lipid test panels), is that LDL-C particles also vary in size – from large, fluffy molecules to smaller and more dense molecules. You can read more about cholesterol from Dr Axel Sigurdsson here: (A well researched blog indeed!). In short, the higher the number of smaller, more dense LDL-C molecules circulating in an individuals system, the higher the risk of developing atherosclerosis and heart disease.

Now, there is a plethora of research studies out there over the last 15 odd years which have compared low-fat/low-carb/high-protein diets amongst both healthy and obese subjects (take a read of the references at the end of this article), however, although average results demonstrate that on balance, ketogenic and low-carb, high fat diets are greatly beneficial with regards to lowering LDL cholesterol and weight – there are in fact outliers in almost every one of these studies. This remains a topic of debate – as does the medical importance of cholesterol in determining risk of heart disease.

From the reading I have done, possible explanations for increased LDL cholesterol following a low-carbohydrate diet include the following:

– Stress, illness and injury
– Infections, gut flora imbalance and leaky gut
– Familial hyperlipidemia
– Hypersecretion of cholesterol from the liver due to increased consumption of saturated fat
– Choline and/or copper deficiency
– Clinical hypothyroidism or sub-clinical hypothyroidism as a result of removing dietary carbohydrates – i.e. chronic restriction of carbohydrate can lead to poor thyroid function manifested by low T3 (a potent thyroid hormone), subsequently causing decreased LDL receptors and hence elevated serum cholesterol level.

Any one of these reasons above provide possible explanations as to why some individuals including myself, experienced negative results following a low carbohydrate diet – please refer to the adjoining references for more info. As I have did not perform further blood tests, I cannot make a foolproof conclusion as to why I was worse-off in this situation. However, my bet is on thyroid function because of the unmistakable feeling that my body felt as though it was in “hibernation” mode. Have a read of the references below and make up your own minds…

– Vreugdenhil, A. C. E., Snoek, A. M. P., van ‘t Veer, C., Greve, J.-W. M., & Buurman, W. A. (2001). LPS-binding protein circulates in association with apoB-containing lipoproteins and enhances endotoxin-LDL/VLDL interaction.Journal of Clinical Investigation, 107(2), 225–234
– Horton, J. D., Cuthbert, J. A., & Spady, D. K. (1993). Dietary fatty acids regulate hepatic low density lipoprotein (LDL) transport by altering LDL receptor protein and mRNA levels. Journal of Clinical Investigation, 92(2), 743–749
– Tosco A et al. Molecular bases of copper and iron deficiency-associated dyslipidemia: a microarray analysis of the rat intestinal transcriptome. Genes Nutr. 2010 Mar;5(1):1-8.
– Harvey LJ, McArdle HJ. Biomarkers of copper status: a brief update. Br J Nutr. 2008 Jun;99 Suppl 3:S10-3.
– Juan J. Díez, Pedro Iglesias. (2014) Serum cholesterol and triglyceride levels in diabetic patients with subclinical hypothyroidism. Endocrinología y Nutrición (English Edition) 61, 419-425
– N. Silva, O. Santos, F. Morais, I. Gottlieb, M. Hadlich, T. Rothstein, M. Tauil, N. Veras, M. Vaisman, P. d. F. Teixeira. (2014) Subclinical hypothyroidism represents an additional risk factor for coronary artery calcification, especially in subjects with intermediate and high cardiovascular risk scores. European Journal of Endocrinology 171, 327-33