The Science of Nutritional ketosis in LCHF diet

Easier reading of the excerpts at my google document. 


To go to the original article see:

Front Psychol. 2015; 6: 27.

Published online 2015 Feb 2. doi:  10.3389/fpsyg.2015.00027

Excerpt One 

"There are two distinguished types of food intake regulation:

a) the short-term (satiety signals, SS) occurring at the beginning and end of a single meal;
it also includes the length between meals and

b) the long-term regulation (adiposity signal, AS) that is influenced by such factors
as body fat deposition."

Excerpt two

"Hormones like leptin and insulin, both secreted into the blood,
reflect the stored body fat.
These hormones can pass the BBB and stimulate specific receptors.
Hypothalamic areas are richly supplied by axons from ARC,
which has greater concentrations
of leptin and insulin receptors than any other hypothalamic site (Valassi et al., 2008).

The ARC exerts opposing actions on food intake responding not only to leptin and insulin,
but also to gut hormones (the most studied are ghrelin and, recently, PYY).
The neurophysiological pathways suggest that feeding is regulated by a feedback loop,
where the hypothalamus provides the long-term regulatory input to the NTS,
which acts as a setpoint (Williams et al., 2001).

It has recently been proposed that the ARC is required for the
coordination of homeostatic circadian systems including temperature and activity."

Excerpt three

Many molecules produced by the GIT exert hunger or satiety effects on the brain."

Ghrelin

Cholecystokinin (CCK) Three other related hormones are

1- pancreatic polypeptide (PP),

2- amylin, and

3- peptide YY (PYY).

Amylin Peptide YY (PYY)

glucagon-like peptide 1 (GLP-1)

"The gut-brain link is important not only for the hormones produced by the gut,
but also for the long-term body weight regulation."

Excerpt four


"It is important to note that during physiological ketosis (fast or very low calorie ketogenic diets)
ketonemia reaches maximum levels of 7–8 mmol/L
with no change in blood pH,
while in uncontrolled diabetic ketoacidosis blood concentration of KBs can exceed 20 mmol/L
with a consequent lowering of blood pH
(Robinson and Williamson, 1980; Cahill, 2006) (Table ​(Table11).

We can say that no species, including humans,

could have survived for millions of years without the ability to withstand
brief periods of hunger or starvation (Amen-Ra, 2006).

These periods of fasting are themselves ketogenic (McCue, 2010)
during which the concentrations of insulin and glucose decrease

while that of glucagon increases in the attempt to maintain normal blood glucose levels.

When the body passes from a condition of food abundance to one of deprivation
(or else via VLCKD simulated deprivation), there is, with a slight delay,
an increase in the concentration of free FAs as well as KB in the blood.

Thus,
from this point of view KD could be compared to caloric restriction for fasting. "

Excerpt five

Effects of ketosis on hunger and satiety

"Although convincing, the bulk of evidence
in relation to the inhibitory effects of ketosis on appetite is still anecdotal.

Preliminary scientific reports seem to support this phenomenon,
and the evidence shows that KD is more effective,
at least in the short/medium-term, on fat loss (Paoli, 2014).

It was demonstrated that diet-induced weight loss
leads to changes in energy expenditure and in appetite-regulating hormones
that facilitate weight regain and the return to initial energy homeostasis
(Sumithran et al., 2011).

This response to alteration of energy balance
nullifies the success of many dietary approaches.

It is well-known that the long-term success of a nutritional approach is defined
by the amount of weight regain and is the main problem
regarding the so-called weight cycling or “yo-yo” effect (Jeffery, 1996).

A recent study by our group has demonstrated that a brief ketogenic period,
if followed by a longer period of correct Mediterranean diet
could avoid this yo-yo effect (Paoli et al., 2013)."

INSERT:Brian Edwards note: this long term study was only 12 months long.

Excerpt six

"Recently, Sumithran et al. demonstrated that there is a long-term persistence of changes
in some peripheral hormones involved in food control (Sumithran et al., 2011).
In this study,
they found a significant difference in mean levels of many food intake-related hormones
1 year after the cessation of weight loss via the hypocaloric diet.
There was a long lasting decrease of anorexigenic compounds:
1-leptin,
2-PYY,
3-cholecystokinin,
4- insulin, and
5- pancreatic peptide and an
6-increase of the orexigenic molecule ghrelin.
Moreover,
they found that hunger remained elevated 1 year after diet cessation.
In a successive study the same group investigated hunger-related hormones
after 8 weeks of KD, demonstrating that during ketosis the increase of ghrelin
(a strong stimulator of appetite) was suppressed (Sumithran et al., 2013).
These results are consistent with those of Ratliff et al (Ratliff et al., 2009),
who found no significant change in fasting plasma ghrelin after 12 weeks of VLCD."

Excerpt seven

"The global picture is complicated by the contradictory role of ketosis on
anorexigenic and orexigenic signals (summarized in Figure ​Figure4).4).

Ketones (mainly BHB) can act both orexigenically or anorexigenically."

INSERT my comment: Insulin acts peripherally anabolic, and centrally catabolic.
Leptin and Insulin act on the same pathways centrally. (i.e on inhibiting Ghrelin)