Typically, a low-carb diet will be high in fats. There is no obvious reason to compensate with higher levels of protein.
Ansel Keys fudged his data in the 1950's (the Seven Countries Study) to implicate saturated animal fat in cardiovascular disease. What followed was the dominance of corn oil & other polyunsaturated fats; the pressure from that industry to purge other forms of saturated fats (coconut oil & palm oil) from commercially baked goods; & ultimately, the demonization of fat itself.
In a society where No-Fat & Lo-Fat products are common, a high-fat diet is a hard sell.
The classic low-carb, high-fat diet is used in the treatment of children with epilepsy [1] [2].
"The ketogenic diet initially was developed in the 1920s in response to the observation that fasting had antiseizure properties [1]. During fasting, the body metabolizes fat stores via lipolysis and then the fatty acids undergo beta-oxidation into acetoacetate, β-hydroxybutyrate, and acetone—ketone bodies the cell can then use as precursors to generate adenosine triphosphate (ATP)."
It has a good track record & is safe. In a high-carb diet, the fuel for cells is glucose. In a high-fat diet the fuel will largely be ketones. The difference has a huge impact in the brains of children with epilepsy - far fewer seizures, & complete absence in 10-15%. & the brain is quite happy with ketones as fuel.
It works for adults too, but is considered to be difficult to adhere to, so is rarely suggested.
A high-protein diet is not ketogenic, since protein (as fuel) converts to glucose.
The internet is full of references to sugar feeding cancer. It's true that most cancer cells prefer glucose for energy. The cells take up more than normal cells, because of the demands for rapid cell division - the availability of glucose does not affect demand. There is a theory that with a ketogenic diet, normal cells would just fine, but cancer cells would be at a severe disadvantage, being commited to glycolysis.
"Malignant rapidly growing tumor cells typically have glycolytic rates that are up to 200 times higher than those of their normal tissues of origin. This phenomenon was first described in 1930 by Otto Warburg and is referred to as the Warburg effect. The Warburg hypothesis claims that cancer is primarily caused by dysfunctionality in mitochondrial metabolism, rather than because of uncontrolled growth of cells. A number of theories have been advanced to explain the Warburg effect. One such theory suggests that the increased glycolysis is a normal protective process of the body and that malignant change could be primarily caused by energy metabolism." [3]
This does not apply to PCa cells, which mostly prefer fatty acids for energy. However, a ketogenic diet would restore insulin sensitivity & tend to lower circulating insulin levels. Insulin is a growth factor for PCa.
The strictest ketogenic diet for epilepsy is a 4:1 ratio of fats:(carb + protein) ... grams, not calories.
In 2006, Steve Freedland (Duke University Medical Center) asked: "Is there a role for a low-carbohydrate ketogenic diet in the management of prostate cancer?" [4]
Alas, there is no free text. I mention it because everything Freedland puts his name to is worth reading. Here he is again in 2013 [5].
"While traditionally a low fat diet was thought to be optimal, we previously hypothesized that a reduced carbohydrate diet was likewise beneficial [4]. In a prior study we found that mice consuming a no-carbohydrate ketogenic diet (NCKD) had increased overall survival and slower tumor growth, compared to mice on a western diet, a benefit not observed in mice consuming a low fat diet [6]. "
"we recently tested low-carbohydrate diets (10 and 20% carbohydrate kcals, respectively) vs. a NCKD in a mouse xenograft model and found all carbohydrate restricted diets had similar effects on tumor growth, overall survival, and IGF axis signaling, suggesting that low carbohydrate diets may be as effective as a NCKD [7]"
"While these dietary changes appear to be promising for slowing tumor growth, the best established therapy for stunting PCa involves chemical or surgical castration. The deleterious effects of androgen deprivation on weight, diabetes and cardiovascular health make dietary decisions under this circumstance of particular interest. Thus we sought to explore the effect of low- and no-carbohydrate diets on tumor growth and survival as an adjunct to androgen deprivation therapy in a PCa xenograft model."
"In general, mice fed a western diet had the shortest survival, while those on a 20% carbohydrate diet had the slowest tumor growth and thus the subsequent longest survival"
"Carbohydrate restriction provided a benefit to slowing PCa tumor growth compared to a western diet in castrate mice. Our data suggest that diets achievable in humans (e.g., 20% carbohydrate restriction) may play a role in PCa management. Human studies are underway."
In a 2014 Swedish paper [8]:
"a {low carbohydrate-high protein} diet was associated with lower prostate cancer incidence."
The next study (2014 - Canada) [9] considered "low carbohydrate (CHO), high protein diets":
"in longer-term studies using male Transgenic Adenocarcinoma of the Mouse Prostate mice, which are predisposed to metastatic prostate cancer, the 15% CHO diet, with and without celecoxib (0.3 g/kg chow), gave the lowest incidence of metastases, but a more moderate 25% CHO diet containing celecoxib led to the best survival."
"Over 80 years ago, Otto Warburg found that rapidly dividing cancer cells, unlike normal cells, rely more heavily on glycolysis than OXPHOS, even under normoxic conditions, to meet their metabolic needs. This is likely because glycolysis does not catabolize glucose completely to CO2 for ATP but instead uses the carbon skeletons as building blocks for nucleic acid (i.e. ribose) and protein (i.e. alanine, etc.) synthesis, which are essential for cell proliferation. However, because glycolysis is far less efficient at generating ATP, most cancer cells require higher levels of glucose than normal cells to proliferate and survive. Therefore, as long as cancer cells can obtain high levels of glucose, a high glycolytic rate provides both sufficient ATP and glucose-derived carbons, even under hypoxic conditions, for tumor cell survival and proliferation. In earlier studies, we demonstrated that we could lower BG, insulin and lactate levels with isocaloric low CHO, high protein diets and that these diets both slowed tumor growth and reduced cancer incidence and this effect was additive with the COX-2 inhibitor, celecoxib."
-Patrick
[1] ncbi.nlm.nih.gov/pmc/articl...
[2] ncbi.nlm.nih.gov/pmc/articl...
[3] en.wikipedia.org/wiki/Glyco...
[4] ncbi.nlm.nih.gov/pubmed/168...
[5] ncbi.nlm.nih.gov/pmc/articl...
[6] ncbi.nlm.nih.gov/pmc/articl...
[7] ncbi.nlm.nih.gov/pmc/articl...
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