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Comment on ”Ketoacidosis associated with low-carbohydrate diet in a non-diabetic lactating
woman: a case report"
Csaba Tóth
(2015-10-20 15:34) Paleomedicina Hungary Ltd., Budapest, Hungary
I became curious when I read the title of the case report by drs. Geijer and Ekelund. I am using a low carbohydrate diet, we refer to as the
paleolithic ketogenic
diet, in the treatment of diverse chronic diseases already for six years [1-6]. I have to say that in my practice I did
never see a single case where ketoacidosis or
metabolic acidosis developed while on the paleolithic ketogenic diet, even though I am familiar
with the diagnosis and treatment of these conditio ns given my 5-years experience in ICU.
In my reply I would like to comment on the case presented and to clarify some common misunderstandings related to ketosis whi ch are also
reflected in this report.
First, lactation itself does not predispose to ketosis. Whether ketosis develops in a healthy lactating woman only depends on the type of the
nutrition. In newborn
infants, however, ketosis is achieved within a few hours after birth and they remain so while breastfeeding. There is
ample evidence showing that the state of
ketosis is not abnormal but physiological at any age. For example, indigenous people of the Arctic
following a traditional fat-meat based diet containi ng little or no
carbohydrate are in ketosis through their entire lifespan. Our experience with
patients also indicates that eve n a prolonged full fat-meat diet does neither predispose
to ketosis or metabolic acidosis. Given these facts the
explanation for the pheno menon described in the report of drs. Geijer and Ekelund lies elsewhere.
It is important to emphasize that low carbohydrate diets can only be mai ntained on the long term when the diet is high in fat. Yet, in the case
report it is not detailed
how the authors ascertained whether the diet was indeed high in fat and what exactly the patient was eat ing. Other
important details were not mentioned either such
as the weight or BMI of the patient. This is an important issue given that loss of 4 kg within
10 days in a thin patient should be reg arded as starvation. In an obese
patient, however, such a weight loss simply reflects loss of retained
water but not starvation. It is also not mentioned whether breath acetone was detectable or not,
an important characteristic of ketoacidosis.
In the following I put forward those possible scenarios which alone or i n combination may explain the development of the condition described
in the patient.
1.
Any diet with low fat-low carbohydrate content
Given the unreli able sources on the internet, lack of full appreciation of nutrition basics, lack of professional guidanc e as well as fear from
fats, it may occur that a
patient on a low carbohydrate diet does not eat fat in enough quantities. Given that energy comes either from fat or
glucose these patients are indeed starving. Low
fat-low carbohydrate diets are not sustainable on the long term. This is especially the case in
lean patients with low fat reserves. This condition may lead to mild
acidosis and some of the symptoms mentioned in the report.
2.
The classical ketogenic diet
The classical ketogenic diet (and some close variants) has long b een used for nearly a century in the treatment of epilepsy and thus
considerable experience has been gathered with its use. It is well-recognized that the classical ketogenic diet is associated with side effects
some of which were also seen in this patient including
mild acidosis, nausea, vomiting, cramps and malaise. Importantly, in the classical
ketogenic diet the blood ketone concentration desired for adequate epilepsy
control is above 6 mmol/l which is quite close to the 7.1 mmol/l
ketone concentration of the patient. In the ketogenic diet literature there is general agreement that
only ketone concentrations above 15
mmol/l are regarded as cause for concern for severe metabolic acidosis [7]. It is also important to mention that side effects of
the classical
ketogenic diet (and also in the majority of the popular low carbohydrate diets) are not comi ng from ketosis but dietary components
(unhealthy
vegetable oils, either polyunsaturated or saturated, and dairy).
3.
Consumption of foods (e.g. meat products) with additives
Tachycardia and malaise may be caused by food additives including nitrites and nitrates as well as sodium glutamate. Nausea and womiting
may also develop
following increased intake of meat products contaminated with dioxin, an underestimated issue associated with products of
the food industry.
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4.
Abrupt shift toward a low carbohydrate diet
Nausea, womiting, headache and alterations of blood gas (low grade acidosis) may also develop if one shifts toward a low carbohydrate diet
from a high
carbohydrate diet abruptly. Symptoms may persist for 5-10 days and then are resolving spontaneously. These transitory
side-effects are well-known and are explained by the fact that adaptation to a fat-based metabolism, which involves the upregulation of some
mitochondrial enzy mes, takes some time. Given that in the
present case only 10 days have passed since dietary shift this may point to an
incomplete adaptation.
5.
Excessive carbohydrate int ake followin g starvation or low carbo hydrate diet
The phenomenon that excessive carbohydrate intake following prolonged starvation may caus e acidosis is well-documented and is explained
by the relative
shortage of insulin while in a fat-adopted state. In particular, such cases were ob served after the second world war when the
concentration camps were liberated, and those who had been starving before rec eived larger amounts of carbohydrate. Abrupt
carbohydrate load in thes e cases may cause acidosis, headache, vomiting
and hypotonia. Even death in some cases . A similar, althoug h
less severe condition is seen in those preg nant women who previously had been following a low
carbohydrate diet undergo glucose
tolerance test as part of their routine screening. In these cases mild nausea, acidosis and resulting low blood glucose may
emerg e.
Importantly, in the present case the meas ured low lev el of blood glucose does neither preclude carbohydrate intake given that, for
example, fructose does
not elevate blood glucose.
I suppose that any of the above situations, but most probably the fifth one, may more parsimoniously explain the condition de scribed in the
patient as compared to
low carbohyd rate-high fat diet which has never been described to result in ketoacidosis in non-diabetic subjects. In
addition it seems probable that the patient was
consuming larger amounts of vegetable oils before admission to hospital. This is indicated by
the constellation of low thyroid hormones but normal TSH. Starvation
only should have resulted in low thyroid hormones along with low TSH.
The link between vegetable oils and decreased thyroid hormones is well-described in the
literature [8] and our experience indicates that this
also applies to coconut oil which instead of animal fats is commonly advoc ated by low carbohydrate proponents.
Hypothyreosis in the past
medical history of the patient also points to increased regular intake of vegetable oils. Given that thyroid hormones affect the synthesis of
proteins cons umption of vegetable oils may decrease the synthesis of insulin and that of the proteins of mitochondrial enzymes. In the
present case consumption of
vegetable oil might have hindered adaptation to the low carbohydrate diet.
I suppose that in the present case an adequate ratio of fat to protein and the exclusive use of animal fat might have been able to rev erse
the acidosis and
associated symptoms. As detailed earlier consumption of vegetable oils may prolong time required to adaptation to a fat
based metabolism. During this period the
patient may feel fatigue and malaise and therefore may feel need to consume carbohydrates
thinking to help the situation. However, an opposite effect may be
achieved.
Referenc es
1.
Clemens Z, Kel emen A, Fogaras i A, Tóth C. Childhood absenc e epilepsy successfully treated with the paleolithic ketogenic diet. Neurol Ther. 2013;2:71–6.
2.
Tóth C, Clemens Z. Type 1 diabetes mellitus successfully managed with the paleolithic ketogeni c diet. Int J Case Rep Images. 2014;5:699–703.
3.
Tóth C, Clemens Z. Successful treatment of a patient with obesity, type 2 diabetes and hypertension with the paleolithic keto genic diet. I nt J Case Rep Images.
2015;6:161–167.
4.
Tóth C, Clemens Z. Gilbert’s syndrome successfully treated with the paleolithic ketogenic diet. Am J Med Case Rep . 2015;3:117–120.
5.
Clemens Z, Kel emen A, Tóth C. NREM-sleep Associated Epil eptiform Discharges Disappeared Following a Shift toward the Paleolithic Ketogenic Diet in a Child with
Extensive Cortical Malformation. Am J Med Case Rep. 2015;3:212–215 .
6.
Clemens Z, Dabóczi A, Tóth C. The paleolithic ketogenic di et may ensure adequate magnesium levels. Med Hyp. 2015 (accepted for publication)
7.
Volek SF, Phinney SD. The art a nd science of low carbohy drate performance. Be yond Obesi ty LLC 2011
8.
Vazquez JA, Kazi U, Madani N. Protein metabolism during weig ht reduction with very-low-energ y diets: evaluation of the independent ef fects of protein and
carbohydrate on protein sparing. Am J Clin Nutr. 1995;62:93–103.
Competing interests
No competing interests
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