A better title would have been the effects of an inflammatory diet of 40% milk casein and 10% sugar by weight but that wouldn’t be as effective at scaring people from cutting back on carbs…
https://www.jstage.jst.go.jp/article/jnsv/65/Supplement/65_S67/_pdf/-char/en
That does it, no more KETO for me. I don’t want my fur looking that manky! 
They are using Lard; is that hydrogenated lard?
Over 50 calories seems to be the cut off point for mice and maybe humans for longevity or lifespan variables?
So the lower the calories are in ratio to carbohydrates are to protein and fat are restricted or increased to that cut off point or tolerance thereof will increase longevity? (at least in mice?)
Maybe the nutrient density prior to fasting?
“…Autophagy, along with the ubiquitin–proteasome system, is a major intracellular system for protein degradation. It is a large-scale degradation system that uses the enzyme lysosome to degrade cytoplasmic structural components.
This degradation system is known to be involved in processes such as the degradation of proteins that are damaged by stress (30–33). In addition to nutrient starvation, autophagy is induced by endoplasmic reticulum stress, hypoxia, and oxidative stress caused by unfolded proteins and by bacterial and viral infections.
Its mechanism is closely related to the intracellular signal transmission system. In recent years, analysis of mice incapable of autophagy has shown that autophagy contributes to the prevention of various aging-related diseases, including neurodegenerative diseases and tumor formation, since decreased autophagic activity reduces inflammation and aging (34–36).
In our study, measurement of serum IL-6 level, an indicator of autophagic activity and inflammation in the skin, suggested that the mice fed the carbohydrate-restricted diet demonstrated inhibited autophagy and aggravated inflammation (Table 2).
Autophagy is regulated by mTOR (37, 38), and in a nutrient-rich environment, it is inactivated by mTOR-induced direct phosphorylation of autophagy related factors.
Under nitrogen starvation, mTOR activity decreases, causing the molecules to dephosphorylate and activate downstream autophagosome formation. In our study, we observed strong mTOR activation in mice fed with the carbohydrate-restricted diet (Table 2).
These findings demonstrate that long term carbohydrate restriction promotes skin senescence in SAMP8 mice through mTOR activation.
When protein content in the body increases, as in a carbohydrate restricted diet, it leads to high blood concentrations of valine, leucine, and isoleucine, which are branched-chain amino acids (BCAA) (39). BCAA activates mTOR and its downstream pathway (40); consequently, the amount of protein and carbohydrates in the diet greatly affects mTOR activation. mTOR activation, in turn, has been reported to shorten the lifespan of the mice, while its inhibition has been reported to extend it (16, 41, 42). Under a 30–50% calorie restriction, the decreased intake of protein and carbohydrates inhibits mTOR, delays senescence, and extends lifespan (43).
Therefore, if the mice were not fed ad libitum, as in this study, but rather given a carbohydrate-restricted diet on a restricted feeding plan, it is possible that senescence may not have been promoted.
When protein content in the body increases, as in a carbohydrate-restricted diet, it leads to high blood concentrations of valine, leucine, and isoleucine, which are branched-chain amino acids (BCAA) (39). BCAA activates mTOR and its downstream pathway (40); consequently, the amount of protein and carbohydrates in the diet greatly affects mTOR activation.
mTOR activation, in turn, has been reported to shorten the lifespan of the mice, while its inhibition has been reported to extend it (16, 41, 42).
Under a 30–50% calorie restriction, the decreased intake of protein and carbohydrates inhibits mTOR, delays senescence, and extends lifespan (43)ii. Therefore, if the mice were not fed ad libitum, as in this study, but rather given a carbohydrate restricted diet on a restricted feeding plan, it is possible that senescence may not have been promoted.
Carbohydrate restricted diets completely contrast the carbohydrate centric meals typical of the Japanese diet.
If carbohydrate restricted diets are indeed effective in delaying senescence, then Japanese foods can be improved further to include similar health benefits. However, carbohydrate restriction did not have any beneficial effects on longevity in our study.
One of the characteristics of the Japanese diet that is effective in promoting longevity is that it uses a variety of ingredients without leaning heavily toward specific ingredients (12).
However, in contrast to Japanese diets, the carbohydrate restricted diets are extremely high in protein and fat, which leads to imbalanced nutrition.
Previous studies have reported increased mTOR activation with increasing protein-to-carbohydrate ratios (16). Thus, carbohydrate restriction in a low-carbohydrate, high protein diet was found to be ineffective for longevity, as chronic mTOR activation.
**We previously tested using a high-fat diet that contained a large amount of lard in a similar manner to this study and showed that the high-fat diet promoted aging (17). In this study, the carbohydrate restricted diet accelerated aging more than the previous high-fat diet results. Thus, it is possible that a large amount of lard and carbohydrate restrictions acted synergistically to promote aging.
Recently, a large-scale epidemiological study reported that high carbohydrate intake leads to high mortality rates and increased risk of cardiovascular diseases (44). However, the study did not observe a definite connection between low intake of carbohydrates (50% calories) and health, and rather than promoting intake of low carbohydrate diet, concluded that moderate intake of carbohydrates is optimal.
There is no statistically significant difference in carbohydrate intake and mortality rate in Asia, where the carbohydrate intake is high.
The mortality rate is extremely low when carbohydrates are composed of approximately 60% calories, forming a U-shaped curve. In Asia, negative effects were observed when carbohydrate intake was < 50% for >70% calories.
In our previous study, we observed that the life-span of mice was shorter when administered the 1960 Japanese diet, in which the carbohydrate content was 70% calories (11). Thus, we conclude that carbohydrate intake of > - 70% calories is ineffective for longevity. In addition, while there is a large regional disparity in the effects of carbohydrate intake, it is important to demonstrate the proportion of calories that is safe for carbohydrate intake over a long-term period.
We suggest that more research data should be accumulated, particularly on humans, in cases where carbohydrate intake is > - 50% calories. …” …More
Footnotes:
[1] mTOR and its downstream pathway are activated in the dorsal root ganglion and spinal cord after peripheral inflammation, but not after nerve injury. …More
Now I will know what I should and shouldn’t feed my nice 
lol
