“Just because your hypothesis relies on ‘evolution’ doesn’t make you anymore right than anyone else” - Mat Lalonde
Some in the ancestral/alternative health community may be attracted to evolutionary theories of disease, and agree with them even when the evidence doesn’t support the arguments or the conclusion*.
I’ve discussed the thriftygene hypothesis**, which proposes obesity, a chronic disease, is evolutionarily adaptive***. While the observations are correct, the explanations have a lot of counter-evidence against them and alternative explanations seem more accurate.
There are other evolutionary theories of disease that propose a particular chronic disease is evolutionarily adaptive. For example:
* Some may also automatically consider Paleo to be the right approach to eating just because it uses evolution. Even if it’s true, the argument is invalid
** The thrifty gene hypothesis suggests some people have thrifty genes that promote overeating and weight gain during times of plenty to prepare them for famines, and that because famines no longer occur these people gain weight
*** Weight gain could be a physiological adaptation to energy overload mediated by low level mitochondrial dysfunction, ER stress, PTP1B, therefore minor leptin resistance to enable excess calories to be stored as fat. But physiological adaptation is different to evolutionary adaptation.
“…adolescent acne is a normal physiological process - a high-order psychoneuroimmune interaction - that functions to ward off potential mates until the afflicted individual is some years past the age of reproductive maturity, and thus emotionally, intellectually, and physically fit to be a parent.” 
Acne shouldn’t be necessary for this function. Cultural norms and other cues could ward of potential mates and the difference in appearance between 12-14 year olds and ~20 year olds is a signal of maturity. There are some problems with this idea:
- No cases of acne have been found among hunter-gatherers and lower rates of acne are observed in rural, less westernised groups 
- Acne affects young adults as well and can persist into middle age
- Severe acne can cause semi-permanent scarring
- (Not all adolescents are/have been affected by
Androgens for sebum production and bacteria both seem necessary for acne . But plausible underlying pathologies of acne include: hypochloridia, leaky gut, dysbiosis, LPS, chronic stress, low Treg cells/IL-10 and inflammation. These underlying pathologies are a more plausible explanation of acne and may explain the associations between acne and other chronic disease  , the absence of acne among hunter-gatherers and the prevalence among modern industrialised societies
There are others like this which I’ll tackle in future posts
A General Genetic Argument
Below is a line of arguing that has been used to suggest depression is evolutionarily adaptive, but can also be used for any other highly heritable chronic disease
- Depression is highly heritable
- Genes that predispose one to depression are still around
- Therefore those genes have not been selected against
- Therefore those genes have been selected for (are evolutionarily adaptive)
- Therefore depression is evolutionarily adaptive
The first conclusion is fine and is one of the points I made in my previouspost. The second and third conclusion do not necessarily follow.
Just because genes haven’t had selection pressures against them doesn’t mean they have had selection pressures for them. Seeing as hunter-gatherers and traditional cultures have near population-wide freedom from chronic disease, genes that promote chronic disease only in the context of western diet and lifestyle haven’t had almost any selection pressure against them, at least in so far as the genes relate to chronic disease.
Just because genes that are associated with chronic disease have been selected for, doesn’t mean the chronic disease has been selected for (that's a false dichotomy). Genes produce proteins that have many effects on the body. Some of these effects may have been beneficial among hunter-gatherers but promote disease in the context of a western diet and lifestyle. A good example is the GG phenotype for myeloperoxidase (MPO), which increases the expression of the MPO gene, therefore generally more MPO. The GG phenotype would have ideal for hunter-gatherers as it enhances immunity but is detrimental now as MPO products can oxidise LDL and HDL and promote atherosclerosis. The argument above could conclude that atherosclerosis and CVD are evolutionarily adaptive. The more likely explanation is that the GG phenotype has had positive selection for its immune effects without negative selection due to CVD.