Even lurking just a bit on fitness communities shows that people often talk about single digit body fat levels.

Intuitively, this does not seem to be a 'normal' state of the body. People with such low fat levels do not necessarily seem healthy on first glance, with their paper-thin skin, prominent veins, and visible facial bones. Anecdotally, I’ve seen a female athlete complaining on the internet that when she was dropping to her lowest fat levels her grandma was asking if she wasn’t sick.

Question arises if such low fat levels are not a health hazard?

I know that athletes often drop fat to the lowest possible levels just days before a competition and, once the competition is finished, return to slightly higher levels. So these lowest possible levels seem unsustainable long-term. Even if the 'normal' low fat levels of athletes are still not low enough to cause health hazards, the question still arises if these periodical drops to even lower levels are not hazardous.

Googling didn’t bring up particularly helpful results: mostly articles about weight loss from being overweight or, in case of results that were about abnormally low body fat levels, questions on how to reach them or posts boasting about having achieved them.

The best I could find was this table from American Council on Exercise, presented without evidence nor much commentary:

Description Women Men
Essential Fat 10-13% 2-5%
Athletes 14-20% 6-13%
Fitness 21%-24% 14-17%
Acceptable 25%-31% 18%-24%
Obesity >32% >25%

Am I to understand that if a man drops to 2% body fat then essential levels are still met and so no short term nor long term ill effects are likely to manifest?

Note that I am asking about body fat levels well below what is usually considered a 'healthy normal' in most people and not about losing fat from being overweight.


1 Answer 1


There is a well documented association between strenuous exercise and menstrual irregularities in women.

Some authors have argued this should not be considered pathological since the effect is temporary and relieved by cessation of exercise so is rather an adaptation to demands placed on the body.

There is also a related condition called the female athlete triad which consists of:

  • osteoporosis
  • amenorrhea
  • disordered eating

Why do we see secondary amenorrhea in these individuals?

FHA manifests from many factors influencing the complex hypothalamic–pituitary–ovarian axis. When energy stores fail to meet the energy requirements of the body, there are numerous downstream effects. At the level of the hypothalamus, gonadotropin-releasing hormone (GnRH) secretion decreases, leading to less follicle-stimulating hormone (FSH), luteinizing hormone (LH), follicular development, and estrogen secretion. Serum testing of FSH and LH levels in a female with FHA falls in the low-normal to pre-pubertal range reflecting this physiologic change. Cortisol and stress affect this axis, as increasing levels of cortisol inhibit GnRH secretion. This action helps to explain why times of high stress can lead to irregular menses and amenorrhea.

So we can see low energy stores causes abnormalities in the female HPG axis.

Males also have a HPG axis so is there a similar situation in the male? There is less literature on this probably owing to endocrine abnormalities having more obvious consequences in women. But the answer appears to be yes.

Cross-sectional reports of hypogonadotropic hypogonadism have been reported in male athletes, particularly in those athletes participating in endurance sports, and include evidence of low testosterone [49–52], poor semen quality/oligospermia [53, 54], and low libido [55, 56].

I recommend reading this paper as there is much more detail than I can include in an answer. However some highlights:

Interestingly, it is primarily in “extreme” situations consisting of high intensity, long duration exercise or simultaneous exposure to multiple stressors that significant reductions in metabolic and reproductive hormones are observed.

In cross-sectional studies of chronic strenuous exercise training, it seems that very high training loads are required for impairments to be translated to the HPG axis, presumably through poor energetic status. We found that high mileage runners (108.0 ± 4.5 km/week), compared to moderate distance runners (54.2 ± 3.7 km/week) and controls, had lower testosterone levels as well as poor semen quality, including decreased sperm motility, an increased immature sperm number, and decreased bovine cervical mucus penetration, all of which are associated with infertility [53]. It is important to note that the moderate mileage runners in our study maintained a gonadal and semen profile that was similar to that of the sedentary control group, despite running approximately 40–60 km/week. We concluded that in male athletes participating in high-volume training, the findings of decreased testosterone and abnormal semen profiles (Table 1) likely reflect the failure of these athletes to increase energy intake in a manner that accommodates the increased energy expenditure associated with a high training volume [53, 54].

So, to summarise, yes there can be pathological effects to these lifestyles. They are chiefly associated with the combination of very low energy input and high energy output in the form of exercise. The effect is more widely seen in women but can occur in males who are engaged in extremely strenuous exercise, especially with concomitant stressors like sleep deprivation and psychological stress. The dysfunction involves disruption of the HPG axis causing either hypoandrogenic or hypoestrogenic states in males and females respectively.

As discussed in this paper hypogonadotrophic hypoestrogenic states in women can result in anovulation and decreased libido which can result in infertility.

Other adverse effects discussed include:

low bone mineral density, osteoporosis and stress fractures, psychologic effects, diminished athletic perfor­mance, and morbidity or even death due to disordered eating patterns

  • 2
    O Maolain Perhaps infertility (in women) should be mentioned. A good review. Boutari C, Pappas PD, Mintziori G, Nigdelis MP, Athanasiadis L, Goulis DG, Mantzoros CS. The effect of underweight on female and male reproduction. Metabolism. 2020 Jun;107:154229. doi: 10.1016/j.metabol.2020.154229. Epub 2020 Apr 11. PMID: 32289345. Your answer is great and no need to add another answer. Jan 10 at 23:07
  • My issue with this answer is the assumption that fertility and menstruation are "the norm". Consider a mind set in which women only become fertile when there is a glut of food, easily obtained. Then none of these observations describe pathology. Also, disordered eating patterns acquired as part of the actions to artificially achieve a low body fat are not side effects of that low body fat, which is what the question asked about. Jan 15 at 12:27

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