Lifetime Impact of Cow’s Milk on Overactivation of mTORC1: From Fetal to Childhood Overgrowth, Acne, Diabetes, Cancers, and Neurodegeneration
Insulinotropic BCAAs of milk are released by milk protein hydrolysis in the intestine and induce postprandial hyperinsulinemia.
That is why the insulinemic index of milk is three times higher than milk’s glycemic index.
Predominantly, whey protein-derived amino acids released after fast intestinal hydrolysis are responsible for the insulinemic effect of milk. Insulin and IGF-1 synergistically activate PI3K-AKT-mTORC1 signaling, growth, and anabolism.
We know from Bella Mitochondria's paper high insulin depletes vitamin d and magnesium.
Higher vitamin d levels are required to inhibit the mTORC1 signaling.
Vitamin D A new player in the world of mTOR signaling
the ability of 1,25(OH)2D to induce DDIT4 and suppress mTOR may further extend the therapeutic applications of vitamin D to include a role as a potential anti-aging factor.
Epidermal mTORC1 Signaling Contributes to the Pathogenesis of Psoriasis and Could Serve as a Therapeutic Target
It could be that inhibition of mTORC1 signalling is the route by which some of vitamin d benefits are obtained. Vitamin D associated with reduced mortality in psoriasis patients. Maintaining natural 25(OH)D status 46-60ng/ml 115-150nol/l is critical to help to improve health of psoriasis patients.

From the paper at the first link we see
"Since the Neolithic revolution, over 10,000 years of preferentially fermented milk (yogurt, cheese) were the predominant milk products consumed by humans. Recent evidence has suggested that microbial fermentation of milk attenuates milk-mediated mTORC1 signaling, extensively reviewed elsewhere"
It is pretty easy to make your own yoghurt at home or kefir if you prefer. It also means cheese is fine.

Perhaps we ought to think about making our own fermented butter and cream if we knew where to get raw milk/cream at a reasonable price.