Lost your mojo? Check your cholesterol level!
High cholesterol and triglycerides aren't just bad for your heart... they can kill your sex life, too!
Let's talk about sex. To be more specific, let's talk about enjoying sex, especially if you're a woman. Because the sad fact is, a lot of women really don't enjoy it, particularly as they get older, even if they're in a loving relationship with a caring partner who knows how to look after them sexually. In fact, female sexual dysfunction (FSD) affects 41 per cent of reproductive-age women worldwide, and up to 60 per cent of postmenopausal women.
(Here's an on-topic but off-colour joke for you:
Q: What's the difference between a clitoris and a pub?
A: 99 per cent of men can find a pub.)
There are many reasons why women may experience a persistent loss of interest in, and pleasure and satisfaction from, sex, including:
Fatigue - for example due to juggling multiple roles, or from interrupted sleep due to taking care of babies and young children at night, or from chronic illness;
Hormonal changes - for example during pregnancy, breastfeeding and menopause (although some women report an increased sex drive during some or all of those life stages);
Stress, depression and anxiety;
Relationship difficulties - for example poor communication, or feeling resentful of, or betrayed by, their partner;
Personal history - for example, of sexual abuse or trauma;
Medications, especially
Antidepressants including selective serotonin reuptake inhibitors (SSRIs) - unfortunately, the effects on sexual function can persist long after discontinuing these drugs, and they may be permanent - as well as tricyclic antidepressants, monoamine oxidase inhibitors and lithium carbonate;
Isotretinoin (Roaccutane), used for treatment of acne;
High blood pressure drugs including diuretics, beta-blockers and alpha-blockers (which are also used for symptoms of prostate enlargement);
The oral contraceptive pill, and the long-acting injectable contraceptive, depot medroxyprogesterone acetate (Depo-Provera) ;
Cimetidine (Tagamet), used for treatment of reflux and stomach ulcers; and
Antihistamines including diphenhydramine (Benadryl), cetirizine (Zyrtec) and loratadine (Claritin/Claratyne).
Chronic illnesses including heart disease, diabetes, cancer, irritable bowel syndrome, multiple sclerosis, arthritis and thyroid conditions.
Dyslipidaemia and female sexual dysfunction
But there's one very common condition associated with female sexual dysfunction that a lot of seemingly well women have, and yet hardly anyone knows about it: hyperlipidaemia - also known as dyslipidaemia - defined as high low-density lipoprotein (LDL) cholesterol and/or low high-density lipoprotein (HDL) cholesterol and/or high triglycerides.
A team of Italian researchers studied sexual function in 556 sexually active premenopausal women who were free of cardiovascular disease and any other known cause of female sexual dysfunction (including the use of any pharmaceutical or recreational drugs). They found that those who had dyslipidaemia were more likely to experience problems with sex than women with lipid levels in the healthy range.
How much more likely? Well, the researchers used the Female Sexual Function Index, a 19-item self-report questionnaire, to measure the six key dimensions of women's sexual function:
Sexual desire,
Arousal,
Lubrication,
Orgasm,
Satisfaction, and
Pain.
Each domain was scored from 0 or 1 to 6, giving a total possible score of 36, with a higher score representing better sexual function.
Using the generally-accepted cut-off for FSD of 26 on the FSFI scale, they found that a staggering 51 per cent of women with dyslipidaemia reported sexual dysfunction, compared to only 21 per cent of women with normal cholesterol and triglyceride levels. The researchers also used a second, more conservative cut-off - the lowest quarter of FSFI scores, which ended up being a FSFI score below 23 - and found that 32 per cent of dyslipidaemic women were affected by sexual dysfunction according to this criterion, vs only 9 per cent of women with healthy lipid levels. On the other hand, 79 per cent of women with a healthy lipid profile also had healthy sexual function (FSFI > 26), compared to only 49 per cent of dyslipidaemic women:
But how does dyslipidaemia mess around with your sex life? Well, it's been known for many years that men with cardiovascular disease are far more likely to suffer erectile dysfunction than men with healthy hearts and arteries. Dyslipidaemia interferes with the function of endothelial and smooth muscle cells in the penis, preventing the dilation of arteries, compression of veins and relaxation of smooth muscle cells that make an erection possible:
What about women, though? Women don't need to have erections to have sex... or do they? It turns out that the first phase of the female sexual response involves engorgement of the clitoris, a process essentially identical to the male erection. Both clitoral erection and the blood flow that prompts vaginal lubrication, which is a key element of sexual arousal, are orchestrated by the same biochemical pathways that regulate erectile function in men:
"Upon sexual stimulation of the female, an increase in blood flow supplied by the dorsal clitoral and cavernosal clitoral arteries fills sinusoids contained in the corpora cavernosa [19,20]. Sexual arousal is determined by vaginal lubrication. The regulation of blood flow and clitoral erectile function is governed by the same nitric oxide/cyclic guanosine monophosphate pathway in women as erectile
function is in men...Atherosclerosis of the arterial bed supplying female pelvic anatomy can lead to decreased vaginal engorgement and clitoral erectile insufficiency syndrome [29], similar to erectile problems in men, resulting in vasculogenic FSD. Indeed, failure to achieve clitoral tumescence may be an important factor in FSD. Moreover, chronic atherosclerotic disease in animal models can cause significant disease of the vagina [32]."
In simple terms, both dyslipidaemia and atherosclerosis in the arteries supplying women's sexual organs, have essentially the same effect on their sexual function as we see in men. What's bad for the gander, is just as bad for the goose.
How do you know if you have dyslipidaemia... and what should you do about it?
The cutpoints used for identifying women with dyslipidaemia were as follows:
LDL cholesterol levels > 4.1 mmol/L (160 mg/dL), and/or
HDL cholesterol levels < 1.3 mmol/L (50 mg/dL), and/or
Triglyceride levels > 1.7mmol/L (150 mg/dL).
Comparatively few dyslipidaemic participants (roughly 20 per cent) had elevated LDL cholesterol, which is unsurprising given that these were premenopausal women. As discussed in Menopausal hormone therapy: Overpromising and underdelivering?, the hormonal milieu of reproductive-aged women keeps LDL cholesterol levels comparatively low; LDL and total cholesterol tend to rise after the menopausal transition. It's very likely that this increase in LDL cholesterol contributes to the higher burden of female sexual dysfunction seen in postmenopausal women, just as elevated LDL cholesterol is strongly associated with erectile dysfunction in men.
The typical Western diet, which draws most of its kilojoules from animal foods and refined carbohydrates, is a recipe for developing dyslipidaemia. Saturated fat (found mostly in animal products) raises LDL cholesterol, although there are marked differences between individuals in the magnitude of the response to saturated fat intake; unfortunately, the people with the most atherogenic lipid profile are the worst affected by high intake of saturated fat.
The major culprit in hypertriglyceridemia is refined carbohydrates, including soft drinks, alcohol, sugar, and starchy foods (refined grains, tubers and their products); on the other hand, carbohydrate from legumes and whole fruit lowers triglycerides.
Unfortunately, many people who have become aware that the Western diet is unhealthy, have jumped on the ketogenic and carnivore diet bandwagons. Big mistake.
Effects of ketogenic and carnivore diet on dyslipidaemia and atherosclerosis
When young, normal-weight women were put on a ketogenic diet for just four weeks, their LDL cholesterol jumped up by 1.82 mmol/L (70 mg/dL) and their apolipoprotein B-100 (ApoB) - an even more accurate measure of atherogenic potential - and their triglyceride levels also rose. Does this ketogenic diet-induced spike in LDL cholesterol actually translate into more atherosclerotic plaque? According to the recently-published results of the KETO-CTA trial, yes, it does.
The KETO-CTA trial was conducted in lean, metabolically healthy people who had low triglycerides, excellent blood glucose control and low inflammation levels, but whose LDL cholesterol was at least 4.9 mmol/L (190 mg/dL) and had increased by half or more since adopting a ketogenic diet. In just one year of strictly adhering to the ketogenic diet, their average total atherosclerotic plaque burden grew by 50 per cent, and the volume of non-calcified plaque ('soft plaque', the type most strongly associated with the risk of heart attacks and strokes) increased by 43 per cent. Those who already had calcified plaque at baseline, had the steepest rise in total plaque burden. These rates of atherosclerotic plaque growth exceed those seen in other studies of patients with diabetes, metabolic syndrome and obesity.
The bottom line is that even if a ketogenic diet helps you lose weight and achieve apparent metabolic health, it will accelerate the growth of dangerous atherosclerotic plaque in your arteries.
While little research has been conducted thus far on the carnivore diet, case reports documenting its harmful effects on blood lipids are beginning to appear in the literature, like this one describing two brothers aged 28 and 33, who presented to a lipid clinic with LDL-C levels of 15 and 17 mmol/L (580 and 657 mg/dL), respectively. The clinic doctors assumed the men were suffering from a genetic condition called familial hypercholesterolemia, but genetic testing revealed that they were not, and their astronomically high LDL cholesterol levels had instead been induced by eating nothing but meat, fish and dairy products for one year. Despite being healthy, lean, fit, muscular and apparently metabolically healthy, carotid ultrasound revealed that both young men had intima–media thickening, suggestive of the early development of atherosclerosis. Other cases with similar clinical findings are documented here.
OK, so the ketogenic and carnivore diets aren't a good bet for preventing or reversing dyslipidaemia. What about statins?
Statins and sexual dysfunction
Statin drugs might seem like a good solution; they most definitely reduce total and LDL cholesterol, stabilise atherosclerotic plaque volume, and in high enough doses, can even cause plaque regression. Problem is, they may reduce libido and impair testosterone production (which plays a major role in sex drive in both males and females), and atorvastatin is credibly associated with erectile dysfunction in males. Wamp, wamp.
Come on, what's the solution?
Now you know what doesn't work, let's talk about what does. First up, you must accept that there are no quick fixes to this problem. If you have sexual dysfunction associated with dyslipidaemia, you're going to need to commit to a comprehensive diet and lifestyle program aimed at reducing LDL cholesterol/apo B, triglycerides, and overall cardiovascular risk. This program may include some or all of the following:
The Portfolio Diet developed by Dr David Jenkins, which is the most effective dietary approach for reducing LDL cholesterol, as demonstrated by multiple randomised, controlled clinical trials;
If you’re a cholesterol hyperabsorber (which you can assess by testing for sitosterol, campesterol, and/or cholestanol), a completely plant-based diet which eliminates all sources of dietary cholesterol;
Restriction or elimination of alcohol, refined starches and sugars, if you have high triglycerides
Supervised long-term fasting, either very low calorie or water-only;
Regular physical activity, particularly endurance training which lowers both apo B and triglycerides;
Regular safe sunlight exposure;
Ensuring adequate sleep;
Regular meditation; and
Avoiding drugs which raise triglyceride levels, including estrogens (oral contraceptives, HRT), androgens (testosterone), some blood pressure medications (thiazide diuretics, alpha and beta blockers), steroids and isotretinoin (Roaccutane).
And of course, you should also be addressing any of the personal and relationship issues that contribute to sexual dysfunction, with the help of a skilled therapist.
Is all that effort really worth it? After all, many women simply accept their impaired sexual function as an inevitable part of growing older. But, as the authors of the study on dyslipidaemia point out,
"Sexual dysfunction is associated with poor health. Sexual problems may be a warning sign or consequence of a serious underlying illness such as diabetes, metabolic diseases, cardiovascular disease, urogenital tract conditions, or cancer."
And beyond that, human adults are inherently sexual creatures. Anything that undermines healthy sexual expression erodes well-being:
"Persistent sexual problems can lead to feelings of inadequacy, relational conflicts, and deterioration in mental health."
Sexual Dysfunction in the Life Cycle of Women: Implications for Psychological Health
So let's make a concerted effort to get past our cultural reticence around talking about sex - particularly in women, and most particularly, in older women. Having a healthy sex life is a vital part of being a healthy human. And now that we know that dyslipidaemia and atherosclerosis undermine sexual function in both males and females, we have the power to turn around one of the most significant factors contributing to personal and relationship dissatisfaction and conflict.
Last thing: This post took me approximately 15 hours to research and write. If you feel you’ve gotten value from it, please consider a paid subscription to help me continue this work: