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Type 1 diabetes mellitus successfully managed with the paleolithic ketogenic diet

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Introduction: Type 1 diabetes mellitus (T1DM) patients are usually instructed to follow a low fat/high carbohydrate diet. A few studies in literature, however, reported metabolic benefits and sustainability of carbohydrate restricted diets. Case Report: Herein, we present a case of a 19-year-old male with newly diagnosed T1DM. The patient was first put on an insulin regime. Twenty days later, he shifted towards the paleolithic ketogenic diet and was able to discontinue insulin. Strict adherence to the diet resulted in normal glucose levels and a more than three-fold elevation of C-peptide level indicating restored insulin production. Currently, the patient is on the paleolithic ketogenic diet for 6.5 months. He is free of complaints, and no side effects emerged. Conclusion: We conclude that the paleolithic ketogenic diet was effective and safe in the management of this case of newly diagnosed T1DM. Marked increase in C peptide level within two months indicates that the paleolithic ketogenic diet may halt or reverse autoimmune processes destructing pancreatic beta cell function in T1DM.
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International Journal of Case Reports and Images, Vol. 5 No. 10, October 2014. ISSN – [0976-3198]
Int J Case Rep Images 2014;5(10):699–703.
Tóth et al. 699
Type 1 diabetes mellitus successfully managed with the
paleolithic ketogenic diet
Csaba Tóth, Zsófia Clemens
Introduction: Type 1 diabetes mellitus (T1DM)
patients are usually instructed to follow a low
fat/high carbohydrate diet. A few studies in
literature, however, reported metabolic benefits
and sustainability of carbohydrate restricted
diets. Case Report: Herein, we present a case
of a 19-year-old male with newly diagnosed
T1DM. The patient was first put on an insulin
regime. Twenty days later, he shifted towards
the paleolithic ketogenic diet and was able to
discontinue insulin. Strict adherence to the diet
resulted in normal glucose levels and a more than
three-fold elevation of C-peptide level indicating
restored insulin production. Currently, the
patient is on the paleolithic ketogenic diet for
6.5 months. He is free of complaints, and no
side effects emerged. Conclusion: We conclude
that the paleolithic ketogenic diet was effective
and safe in the management of this case of newly
diagnosed T1DM. Marked increase in C peptide
level within two months indicates that the
paleolithic ketogenic diet may halt or reverse
autoimmune processes destructing pancreatic
beta cell function in T1DM.
Keywords: Type 1 diabetes mellitus, Ketogenic
diet, Paleolithic-ketogenic diet, C-peptide,
Evolutionary medicine
Csaba Tóth1, Zsófia Clemens2
Affiliations: 1MD, Medical Director, Paleomedicina Hungary
Ltd, Evolutionary Medicine Working Group, Hidász u. 3,
H-1026, Budapest, Hungary; 2PhD, Senior Research Fellow,
Department of Neurology, University of Pécs, Rét u. 2,
H-7623, Pécs, Hungary.
Corresponding Author: Zsófia Clemens, Department of
Neurology, University of Pécs, Rét u. 2, H-7623, Pécs, Hungary.
Ph: 003672535900; Email:
Received: 08 July 2014
Accepted: 31 July 2014
Published: 01 October 2014
How to cite this article
Tóth C, Clemens Z. Type 1 diabetes mellitus
successfully managed with the paleolithic ketogenic
diet. Int J Case Rep Images 2014;5(10):699–703.
Diabetic patients are, generally, recommended to
follow a diet that is low in fat and high in carbohydrates
[1]. Clinical studies, conversely, showed metabolic
benefits conferred by carbohydrate-restricted diets
including the ketogenic diet [2, 3] and the paleolithic
diet [4, 5] in type 2 diabetes. Much less data on the use
of low carbohydrate diets in type 1 diabetes (T1DM)
are available. Two studies by Nielsen et al. showed that
a low carbohydrate diet lowers the need for insulin as
well as the number of hypoglycemic episodes in T1DM
[6, 7]. It was also suggested that a low carbohydrate diet
is sustainable on the long-term [6, 7]. Ketogenic diets
have long been used in epilepsy [8]. There are three
cases in literature, where concurrent epilepsy and T1DM
were treated with the classical ketogenic diet and both
conditions improved [9–11]. Recently, we published
a case of childhood absence epilepsy where seizure
freedom was achieved using a modified ketogenic diet we
refer to as the paleolithic-ketogenic diet [12]. Herein, we
present a case of T1DM, where the same diet resulted in
remission of T1DM as assessed by normalization of blood
glucose levels and elevation in C-peptide level allowing
for discontinuation of external insulin replacement.
A 19-year-old male complained of increased thirst,
polyuria, itchy skin, malaise, and weight loss. The
symptoms were present for about two weeks prior to
International Journal of Case Reports and Images, Vol. 5 No. 10, October 2014. ISSN – [0976-3198]
Int J Case Rep Images 2014;55(10):699–703.
Tóth et al. 700
diagnosis. On November 24, 2013 self monitoring of
blood glucose showed 384 mg/dL. Previous medical
history was unremarkable. Anamnestic data included
consuming of muscle boosting protein through a month
prior to symptom onset. Laboratory assessment on
November 25, 2013 (Table 1) showed elevations in glucose
(218 mg/dL) and HbA1c (9.2%). Testing for glutamic acid
decarboxylase (GAD) antibodies showed positivity
(52 U/mL; normal range 0–10 U/mL) and mild positivity
for pancreatic islet cell autoantibodies (ICAs). C-peptide
level was not measured at this time. He was diagnosed
with T1DM. He was put on insulin replacement therapy
(38 IU of insulin) and standard conventional diabetes
diet with six meals containing 240 grams carbohydrate
daily. He followed this regime for 20 days. While on this
regime his glucose levels fluctuated between 68–267
mg/dL (Figure 1).
Carbohydrate he consuming before was less than 240
grams. Since his malaise did not improve the patient
consulted the first author in December 2013. To ascertain
T1DM laboratory examination of C-peptide was carried
out. C-peptide level of 0.6 ng/mL measured on January
08, 2014 indicated subnormal insulin secretion (Figure
2). The patient was suggested to switch to the paleolithic-
ketogenic diet which he initiated on December 21, 2013.
From this time, he was also taking 5,000 IU of vitamin
D3 but nothing else as supplement. His diet consisted
of meat, organ meat, fat and eggs. In his diet, red and
fat meats dominated over lean meats. He was eating
vegetables in insignificant amounts. His diet had a
ketogenic ratio (fat : protein + carbohydrate) of at least
2:1. No oil of plant origin or artificial sweeteners were
allowed. The patient was under our close control and
reported daily food records and blood glucose levels.
Upon shifting toward the paleolithic ketogenic diet
glucose levels returned to normal and no major elevations
were seen postprandially either. Insulin was therefore
discontinued. The tapering of insulin was done promptly:
following the first paleolithic-ketogenic meal glucose level
was only 86 mg/dL thus there was no need for external
insulin. Similar blood glucose levels were measured on
subsequent meals on the diet. Thus, the patient required
no insulin subsequently either. Home glucose monitoring
was carried out preprandially as well as postprandially
and tracked once a day for consecutive meals (that is on
consecutive days measures were taken for breakfast, lunch
and dinner, respectively). Average blood glucose level
while on the standard diabetes diet with insulin was 119
mg/dL while 85 mg/dL on the paleolithic-ketogenic diet
without insulin. Fluctuations in glucose levels decreased
as indicated by a reduction of standard deviation values
from 47 mg/dL on the standard diabetes diet to 9 mg/dL
on the paleolithic-ketogenic diet. Average postprandial
glucose elevation on the standard diabetes diet was 23
mg/dL while only 5.4 mg/dL on the paleolithic-ketogenic
diet (Figure 1).
C-peptide measurement was repeated on the 10th
week of the diet (on March 06, 2014). This indicated
an elevation to a value of 2.2 ng/mL (Figure 2). A
comprehensive laboratory workup carried out on March
14, 2014 indicated normal laboratory parameters with
the exception of total cholesterol and LDL cholesterol
which were slightly elevated. Glucose level was 88 mg/
dL while HbA1c was 5.5% (for all laboratory values see
Table 1). Urinary ketone was positive. On March 21, 2014
antibody testing for ICA showed no change in the mild
Table 1: Laboratory data at the time of diagnosis on a normal diet
(on November 25, 2013) and at 10 weeks after diet initiation,
on the paleolithic-ketogenic diet without insulin (on March 14,
2014). Note the normal level of glucose, HbA1c and low level
of triglyceride while on the paleolithic-ketogenic diet. Dashes
indicate that the given parameter was not measured.
Normal diet Paleolithic-ketogenic diet
WBC 5.9 5.4 G/l
RBC 5.7 5.3 T/l
Hemoglobin 16 15.2 G/dL
Hematocrit 48 45 %
Iron 136.3 98.9 µg/ dL
Thrombocyte 230 150 G/l
Sodium 134 139 mEq/l
Potassium 3.9 3.8 mEq/l
Calcium 9.52 10 mg/dL
Magnesium 2.02 mg/dL
Carbamide 10.6 14.8 mg/dL
Creatinine 0.88 0.97 mg/dL
eGFR >90 >90
Glucose 218 88 mg/dL
Hb1Ac 9.2 5.5 %
Total cholesterol 143 301 mg/dL
HDL cholesterol 54.8 mg/dL
LDL cholesterol 224 mg/dL
Triglyceride 168 111 mg/dL
Uric acid 6.12 mg/dL
GOT 31 19 U/l
GPT 44 18 U/l
GGT 17 16 U/l
Total bilirubin 0.94 mg/dL
TSH 3.53 mIU/l
CRP 1.1 mg/L
Abbreviations: WBC - white blood cell count, RBC - red blood
cell count, eGFR - estimated glomerular filtration rate, HbA1c -
glycated hemoglobin, HDL - high density lipoprotein, LDL - low
density lipoprotein, TSH - thyroid stimulating hormone, CRP
- C-reactive protein
International Journal of Case Reports and Images, Vol. 5 No. 10, October 2014. ISSN – [0976-3198]
Int J Case Rep Images 2014;55(10):699–703.
Tóth et al. 701
positivity measured before and some elevation in GAD
antibodies (86 U/mL). At the time of writing this case
report, the patient is on the paleolithic ketogenic diet for
6.5 months and still exhibit low glucose levels. No side
effects emerged and he is completely free of symptoms.
The patient gave written informed consent for writing
this case study.
This is a first report of T1DM being successfully
managed with the paleolithic-ketogenic diet. In literature,
a few studies are available on the use of carbohydrate
restricted diet in the treatment of T1DM [6, 7]. Low
carbohydrate diet in these studies resulted in reduced
number of hypoglycemic episodes and also lowered
the need for insulin. In our case, however, insulin
replacement was not just reduced but could be stopped.
Importantly, insulin discontinuation was paralleled by
a marked increase in C peptide level indicating restored
pancreatic insulin production.
Shortly before diabetes onset our patient consumed
muscle boosting protein which contained bovine milk
protein. Consumption of cow’s milk has repeatedly been
shown to increase risk of T1DM [13, 14]. It is suggested
that bovine milk protein may promote autoimmune
processes giving rise to T1DM [15]. Also in two case
reports from literature, where epilepsy was treated
with the classical ketogenic diet, which contains large
amount of dairy, T1DM developed subsequently [9, 11].
A major difference between the classical ketogenic diet
and the paleolithic ketogenic diet is that milk and dairy
are excluded in the latter. We suggest that the paleolithic
ketogenic diet not only normalize glucose levels but
may also halt autoimmune processes mediated by non-
paleolithic substances including milk protein [16].
While on the paleolithic-ketogenic diet glucose levels
remained low both during preprandially and postprandially.
Follow-up laboratory assessment indicated laboratory
parameters remaining in the normal range except for
elevations in total cholesterol and LDL cholesterol. In fact,
these elevations are expected on a diet rich in animal fat
and cholesterol and were also reported in studies with the
classical ketogenic diet [17] as well as in our previous case
of childhood absence epilepsy treated with the paleolithic
ketogenic diet [12]. Moreover, it is now acknowledged that
neither dietary nor serum cholesterol represent a risk factor
for cardiovascular disease [18]. On follow-up antibody
testing ICA remained mildly positive while GAD antibodies
elevated to some extent. Although these parameters are
frequently associated with T1DM they do not seem to be
specific nor indicate progression of disease [19].
Type 1 diabetes mellitus is considered as a lifelong
metabolic condition due to the exhaustion of insulin-
secretory cells of the pancreas. Therefore, T1DM is
generally believed to be untreatable by any diet. There
are indications, however, that residual pancreatic beta
cell functioning may extend well beyond the time of
diagnosis [20]. Nevertheless C-peptide levels decrease
monotonically through years after diagnosis [20]. We are
not aware of any data from literature indicating elevation
of C-peptide resulting from a dietary intervention. A
recent case study of a child with T1DM reported remission
without insulin on gluten-free diet [21]. However, in that
case C-peptide continued to decline while on the gluten-
free diet.
Figure 1: Blood glucose levels while on the standard diabetes
diet containing 240 g carbohydrate with insulin therapy and
while on the paleolithic-ketogenic diet without insulin. Glucose
was measured preprandially and postprandially once a day for
consecutive meals (that is on consecutive days measures were
taken for breakfast, lunch and dinner, respectively). Note low
glucose levels and the absence of major postprandial elevations
while on the paleolithic ketogenic diet. Due to stable glucose
levels through five months, from May 15, 2014 the patient
switched to self-monitoring his glucose levels only once a week.
Figure 2: C-peptide levels shortly after diet initiation (on the
18th day of the paleolithic ketogenic diet) and two months later.
Note the more than three-fold increase in C-peptide within two
International Journal of Case Reports and Images, Vol. 5 No. 10, October 2014. ISSN – [0976-3198]
Int J Case Rep Images 2014;55(10):699–703.
Tóth et al. 702
In the standard care of T1DM insulin is a cornerstone.
It is important to emphasize that the paleolithic-
ketogenic diet as a standalone therapy may be applied
only in those cases with residual insulin secretion. In
cases with no internal insulin secretion the paleolithic-
ketogenic therapy may be only used as an adjunct to
insulin replacement.
We suggest that an intervention with the paleolithic
ketogenic diet in an early stage of the disease with residual
insulin secretion may halt or reverse type 1 diabetes
mellitus (T1DM). Follow-up at sixth month in the case of
our patient is relatively short and the positive results may
appear as a honeymoon effect. However, this term is used
in relation to the beginning of insulin therapy not the end
of it. We believe that with normalized insulin secretion
and a further adherence to the diet the patient may be
managed on the long-term.
Author Contributions
Tóth Csaba – Substantial contributions to conception and
design, Acquisition of data, Analysis and interpretation
of data, Drafting the article, Revising it critically for
important intellectual content, Final approval of the
version to be published
Zsófia Clemens – Substantial contributions to
conception and design, Acquisition of data, Analysis
and interpretation of data, Drafting the article, Revising
it critically for important intellectual content, Final
approval of the version to be published
The corresponding author is the guarantor of submission.
Conflict of Interest
Authors declare no conflict of interest.
© 2014 Tóth Csaba et al. This article is distributed
under the terms of Creative Commons Attribution
License which permits unrestricted use, distribution
and reproduction in any medium provided the original
author(s) and original publisher are properly credited.
Please see the copyright policy on the journal website for
more information.
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Article citation: Tóth C, Clemens Z. Type 1 diabetes mellitus successfully managed with the paleolithic ketogenic
diet. Int J Case Rep Images 2014;5(10):699–703.
Csaba Tóth is General Practitioner from Hungary with 20 years experience in intensive care medicine,
internal medicine and family medicine. He is using the paleolithic-ketogenic nutrition in the treatment
of chronic medical illnesses including diabetes, cancer, autoimmune diseases and epilepsy for ve
years. He is operating private practice in Budapest and in a few other cities in Hungary. In 2013, he
organized a course on evolutionary medicine in the mandatory training of GPs at the University of
Szeged, Hungary. With an evolutionary medical attitude he strives for the full recovery of his patients.
Zsóa Clemens is Biologist and clinical researcher specialized in nutrition, nutritional therapy and
brain research. She earned her PhD in electroencephalograpy of sleep and epilepsy from Semmelweis
University, Budapest, Hungary in 2005. Currently, she is Senior Research Fellow at the Neurological
Department, University of Pécs, Hungary and is also afliated with the Evolutionary Medicine Working
Group of Paleomedicina Hungary Ltd. In international academic journals, she has published 29 research
articles with more than 500 citations. Email: clemenszso
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... The patient's glycated hemoglobin level was 5.5% and his glucose concentration was 88 mg/dL. Although that change could have occurred independently of the diet used, the authors of the study suggest that the evident increase in the C peptide level accompanying insulin withdrawal may indicate the return of insulin production in the pancreas [54]. Many other mechanisms not strictly concerning the autoimmunology process, such as its effect on glucose, insulin, and insulin resistance, are, to a significant degree, common for both types of diabetes. ...
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As common complication of prediabetes, type I and type II diabetes, diabetic peripheral neuropathy (DPN) includes a series of sensory and motor changes associated with slow nerve conduction, nerve degeneration, gate disturbances, pain, and loss of sensation. Although proper glycemic control can prevent DPN progression, these complications remain difficult to clinically treat. Current pharmacological medications have limited effectiveness, creating the need for additional clinical options. Lifestyle interventions hold great promise as the broad spectrum of improvements derived from certain lifestyle changes appears promising to improve diabetes management and DPN. In this chapter, we highlight research that illustrates the consequences of poor diet on DPN and discuss the benefits of lifestyle changes associated with dietary change and/or exercise. Reversal of dietary changes appears to have positive impact on DPN, and we highlight new studies in which a low-carbohydrate/high-fat diet has been used to prevent and/or reverse DPN. In addition, a growing number of basic and clinical studies are revealing how exercise can improve symptoms of DPN. These interventions affect a broad range of cellular and metabolic changes that can lead to improvements in DPN symptoms. These interventions likely involve overlapping cellular pathways but could also improve DPN through unique mechanisms. As approaches using personalized medicine increase, clinical treatments for DPN will need to determine the most impactful interventions that are relevant to specific symptoms in patients suffering from DPN. Lifestyle and dietary interventions should play an important role in these treatment plans and the convergence of shared mechanisms should be a focus of preclinical and clinical research.KeywordsDiabetesKetogenic dietMediterranean dietExercisePhysical activity
Significance: Diabetic peripheral neuropathy (DPN), a complication of metabolic syndrome, type I, and type II diabetes, leads to sensory changes that include slow nerve conduction, nerve degeneration, loss of sensation, pain, and gate disturbances. These complications remain largely untreatable, although tight glycemic control can prevent neuropathy progression. Nonpharmacological approaches remain the most impactful to date, but additional advances in treatment approaches are needed. Recent advances: This review highlights several emerging interventions, including a focus on dietary interventions and physical activity that continue to show promise for treating DPN. We provide an overview of our current understanding of how exercise can improve aspects of DPN. We also highlight new studies in which a ketogenic diet has been used as an intervention to prevent and reverse DPN. Critical issues: Both exercise and consuming a ketogenic diet induce systemic and cellular changes that collectively improve complications associated with DPN. Both interventions may involve similar signaling pathways and benefits but also impact DPN through unique mechanisms. Future directions: These lifestyle interventions are critically important as personalized medicine approaches will likely be needed to identify specific subsets of neuropathy symptoms and deficits in patients and determine the most impactful treatment. Overall, these two interventions have the potential to provide meaningful relief for patients with DPN and provide new avenues to identify new therapeutic targets.
Methylglyoxal (MGO) is a reactive dicarbonyl byproduct of glycolysis implicated in a growing number of neuropathic pain conditions, including chemotherapy-induced peripheral neuropathy, diabetic peripheral neuropathy, and radiculopathy with lumbar disk herniation. Recent studies show success in preclinical models treating these disorders with an interventional ketogenic diet. Here, we tested the hypothesis that a ketogenic diet modifies pathological MGO signaling as a mechanism underlying neuropathy improvement. We found that mice injected with MGO displayed nocifensive behaviors, whereas mice prefed a ketogenic diet were resistant to mechanical allodynia elicited by MGO. In addition, levels of circulating MGO were reduced in ketogenic diet-fed mice and negatively correlated with levels of the ketone body β-hydroxybutyrate (β-HB). Methylglyoxal is normally scavenged by the glyoxalase system, and ketogenic diet-fed mice displayed increased glyoxalase 1 activity compared with chow-fed control mice. Recent studies also suggest that ketone bodies contribute to MGO detoxification, consistent with a negative correlation between β-HB and MGO. To assess whether ketone bodies modified MGO-evoked nociception through direct MGO detoxification, we coincubated either acetoacetate or β-HB with MGO before injection. Mice receiving intraplantar MGO injection exhibit increased nociceptive behavior (lifting, licking, biting, and scratching), which was significantly reduced by coincubation with either acetoacetate or β-HB. Methylglyoxal increased phospho-extracellular signal-regulated kinase-positive cells in the spinal dorsal horn, and this evoked spinal activation was ameliorated by preincubation with acetoacetate or β-HB. These results suggest that a ketogenic diet and ketone bodies ameliorate MGO-evoked nociception, partially through detoxification of MGO, and provide rationale for therapeutic intervention with a ketogenic diet in MGO-driven pathologies.
Autoimmune diseases are complex conditions that are increasing in incidence worldwide. Autoimmune disorders are often associated clinical challenges in regards to clear diagnoses, comorbidities, and effective disease management and treatment strategies. Importantly, research suggests that an individual’s nutritional status and metabolic health, such as the presence of obesity or metabolic syndrome, may play a role in the risk, pathophysiology, and management of autoimmune diseases. Further, adherence to Western or Mediterranean-style dietary patterns, as well as intake of specific macronutrients (e.g., carbohydrates, protein, fatty acids), micronutrients (e.g., vitamin D, selenium, sodium) and non-nutrient dietary factors (e.g., food contaminants, gut microbiome profiles), may modulate autoimmune disease development and complications. Thus, nutritional interventions may represent an effective approach to mitigate risk and support the management of autoimmune disorders.
Dietary interventions are promising approaches to treat pain associated with metabolic changes because they impact both metabolic and neural components contributing to painful neuropathy. Here, we tested whether consumption of a ketogenic diet could affect sensation, pain, and epidermal innervation loss in type 1 diabetic mice. C57Bl/6 mice were rendered diabetic using streptozotocin and administered a ketogenic diet at either three weeks (prevention) or nine weeks (reversal) of uncontrolled diabetes. We quantified changes in metabolic biomarkers, sensory thresholds, and epidermal innervation to assess impact on neuropathy parameters. Diabetic mice consuming ketogenic diet had normalized weight gain, reduced blood glucose, elevated blood ketones, and reduced hemoglobin-A1C levels. These metabolic biomarkers were also improved following nine weeks of diabetes followed by four weeks of a ketogenic diet. Diabetic mice fed a control chow diet developed rapid mechanical allodynia of the hind paw that was reversed within a week of consumption of a ketogenic diet in both prevention and reversal studies. Loss of thermal sensation was also improved by consumption of a ketogenic diet via normalized thermal thresholds. Finally, diabetic mice consuming a ketogenic diet had normalized epidermal innervation, including after nine weeks of uncontrolled diabetes and four weeks of consumption of the ketogenic diet. These results suggest that, in mice, a ketogenic diet can prevent and reverse changes in key metabolic biomarkers, altered sensation, pain and axon innervation of the skin. These results identify a ketogenic diet as a potential therapeutic intervention for patients with painful diabetic neuropathy and/or epidermal axon loss.
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Introduction Childhood absence epilepsy is an epilepsy syndrome responding relatively well to the ketogenic diet with one-third of patients becoming seizure-free. Less restrictive variants of the classical ketogenic diet, however, have been shown to confer similar benefits. Beneficial effects of high fat, low-carbohydrate diets are often explained in evolutionary terms. However, the paleolithic diet itself which advocates a return to the human evolutionary diet has not yet been studied in epilepsy. Results Here, we present a case of a 7-year-old child with absence epilepsy successfully treated with the paleolithic ketogenic diet alone. In addition to seizure freedom achieved within 6 weeks, developmental and behavioral improvements were noted. The child remained seizure-free when subsequently shifted toward a paleolithic diet. Conclusion It is concluded that the paleolithic ketogenic diet was effective, safe and feasible in the treatment of this case of childhood absence epilepsy.
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The very-high-fat ketogenic diet can worsen lipid levels in children with pre-existing hyperlipidemia by increasing serum lipoproteins and reducing antiatherogenic high-density lipoproteins. A retrospective chart review of 160 children treated with the ketogenic diet from September 2000 to May 2011 was performed. Twelve children with pre-existing hyperlipidemia were identified. Lipid levels including total cholesterol, low-density lipoprotein, triglycerides, high-density lipoprotein, and total cholesterol/high-density lipoprotein were measured pre-diet and at 3, 6, and 12 months of treatment. During treatment, there was a significant reduction in mean total cholesterol, low-density lipoprotein, and total cholesterol/high-density lipoprotein. Total cholesterol and low-density lipoprotein were normalized in 8 and 7 children at 6 months; and 9 and 9 children at 12 months respectively. At 6 and 12 months, tot cholesterol/HDL ratio was normalized in 5 and 7 children respectively. Diet modifications were made to achieve healthy lipid levels. By extrapolating the data, it suggests lipid levels can be controlled in children and adults with ketogenic diet treatment.
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Cow’s milk-based infant formulas and cow’s milk consumption in childhood have been suggested to promote the development of type 1 diabetes mellitus and other immune-mediated or neurological diseases. Epidemiological studies in man have led to the hypothesis that introduction of cow’s milk-based infant formula within the first 3 months of life is associated with increased risk of type 1 diabetes mellitus. Furthermore, in animal models of type 1 diabetes mellitus, cow’s milk proteins have been proven to be ‘diabetogenic’. However, the issue seems far from being resolved. Several epidemiological studies and, more importantly, the first prospective trials did not show an association between early exposure to cow’s milk and type 1 diabetes mellitus. In animal models, cow’s milk proteins are modestly and variably diabetogenic, wheat or soyabean proteins in the diet cause higher rates of autoimmune diabetes. In both man and rodents there is increasing evidence that the gut-associated immune system plays a major role in disease development, probably because of disturbed oral tolerance mechanisms. Oral tolerance depends on immunological homeostasis and normal maturation of the gut. These factors are influenced by growth factors and cytokines from breast milk, normal bacterial colonization, infections and diet. All these factors have been proposed as risk factors for type 1 diabetes mellitus. Hence, cow’s milk proteins may provide mimicry epitopes relevant in autoimmunity, as well as destabilizing oral tolerance mechanisms by biologically active peptides. The concept of dietary regulation of autoimmunity does not apply only to cow’s milk protein, but also to other dietary proteins.
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Background Reduction of dietary carbohydrates and corresponding insulin doses stabilizes and lowers mean blood glucose in individuals with type 1 diabetes within days. The long-term adherence for persons who have learned this technique is unknown. To assess adherence over 4 years in such a group the present audit was done retrospectively by record analysis for individuals who have attended an educational course. Adherence was assessed from HbA1c changes and individuals’ own reports. Findings Altogether 48 persons with diabetes duration of 24 ± 12 years and HbA1c > = 6.1% (Mono-S; DCCT = 7.1%) attended the course. Mean HbA1c for all attendees was at start, at 3 months and 4 years 7.6% ± 1.0%, 6.3 ± 0.7%, 6.9 ± 1.0% respectively. The number of non-adherent persons was 25 (52%). HbA1c in this group was at start, at 3 months and 4 years: 7.5 ±1.1%, 6.5 ± 0.8%, 7.4 ± 0.9%. In the group of 23 (48%) adherent persons mean HbA1c was at start, at 3 months and 4 years 7.7 ± 1.0%, 6.4 ± 0.9%, 6.4 ± 0.8%. Conclusion Attending an educational course on dietary carbohydrate reduction and corresponding insulin reduction in type 1 diabetes gave lasting improvement. About half of the individuals adhered to the program after 4 years. The method may be useful in informed and motivated persons with type 1 diabetes. The number needed to treat to have lasting effect in 1 was 2.
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To examine persistence of C-peptide production by ultrasensitive assay years after onset of type 1 diabetes and factors associated with preserving β-cell function. Serum C-peptide levels, a marker of insulin production and surviving β-cells, were measured in human subjects (n = 182) by ultrasensitive assay, as was β-cell functioning. Twenty-two times more sensitive than standard assays, this assay's lower detection limit is 1.5 pmol/L. Disease duration, age at onset, age, sex, and autoantibody titers were analyzed by regression analysis to determine their relationship to C-peptide production. Another group of four patients was serially studied for up to 20 weeks to examine C-peptide levels and functioning. The ultrasensitive assay detected C-peptide in 10% of individuals 31-40 years after disease onset and with percentages higher at shorter duration. Levels as low as 2.8 ± 1.1 pmol/L responded to hyperglycemia with increased C-peptide production, indicating residual β-cell functioning. Several other analyses showed that β-cells, whose C-peptide production was formerly undetectable, were capable of functioning. Multivariate analysis found disease duration (β = -2.721; P = 0.005) and level of zinc transporter 8 autoantibodies (β = 0.127; P = 0.015) significantly associated with C-peptide production. Unexpectedly, onset at >40 years of age was associated with low C-peptide production, despite short disease duration. The ultrasensitive assay revealed that C-peptide production persists for decades after disease onset and remains functionally responsive. These findings suggest that patients with advanced disease, whose β-cell function was thought to have long ceased, may benefit from interventions to preserve β-cell function or to prevent complications.
Accumulating evidence suggests that low-carbohydrate, high-fat diets are safe and effective to reduce glycemia in diabetic patients without producing significant cardiovascular risks. Most of these studies have been carried out specifically restricting carbohydrates, which tends to lead to increased protein intake, thus reducing the ketosis. However, diets that limit protein as well as carbohydrates, entailing a composition very high in fat, appear even more effective to reduce glucose and whole-body glucose metabolism in humans. In animal models, low-carbohydrate, high-protein diets do not produce ketosis or reduce glycemia but rather cause obesity. However, limiting both protein and carbohydrates as in a classic ketogenic diet remarkably reduces blood glucose in animal models of type 1 and type 2 diabetes and reverses diabetic nephropathy. Future studies should assess if ketogenic diets would be effective to reverse diabetic complications in humans.
A 5-year and 10-month old boy was diagnosed with classical type 1 diabetes mellitus (T1DM) without celiac disease. He started on a gluten-free diet after 2-3 week without need of insulin treatment. At the initiation of gluten-free diet, HbA1c was 7.8% and was stabilised at 5.8%-6.0% without insulin therapy. Fasting blood glucose was maintained at 4.0-5.0 mmol/l. At 16 months after diagnosis the fasting blood glucose was 4.1 mmol/l and after 20 months he is still without daily insulin therapy. There was no alteration in glutamic acid decarboxylase positivity. The gluten-free diet was safe and without side effects. The authors propose that the gluten-free diet has prolonged remission in this patient with T1DM and that further trials are indicated.
Cow's milk β-casein has been proposed as a candidate trigger of autoimmunity associated with type 1 diabetes. In this study, cellular and humoral immunity against β-casein was compared to that against other major cow's milk proteins in patients with recent onset type 1 diabetes and control subjects. T cell responses were found against α-casein, β-casein, β-lactoglobulin and bovine serum albumin in both patients with type 1 diabetes (stimulation index: 0.2–22.8, n=23) and control subjects (stimulation index: 0.1–18.2, n=22), with no significant differences between groups. Twelve (52%) patients and nine (41%) control subjects had stimulation indices >3 to at least one protein, including 9 (39%) patients and 4 (18%) control subjects against β-casein, all but one of these also having elevated responses to α-casein. The highest responses (stimulation index >9) were against α- and β-casein in some patients and control subjects who had the HLA DR3 allele. Antibody levels against α-casein, β-casein and β-lactoglobulin were low in both patients (n=59) and control subjects (n=52). Nevertheless, significantly higher IgG binding to both α-casein in ELISA (P=0.02) and β-casein using ELISA (P=0.02) and RIA (P=0.04) was observed in patients aged <15 years compared to control subjects of similar age. No relationship was found between cellular and humoral immunity against individual antigens. These data show that immune responses to cow's milk are not limited to patients with diabetes and not solely against β-casein.
Diabetic ketoacidosis (DKA) is a life-threatening condition and a major cause of morbidity and mortality in children with type 1 diabetes mellitus. The deficiency of insulin leads to metabolic decompensation, causing hyperglycemia and ketosis that resolves with the administration of insulin and fluids. However, an induced state of ketosis is the basis for the success of the ketogenic diet (KD), which is an effective therapy for children with intractable epilepsy. We report the case of a 2-year-old girl who presented to the emergency department with 1-week history of decreased activity, polyuria, and decreased oral intake. Her past medical history was remarkable for epilepsy, for which she was started on the KD with a significant improvement. Her laboratory evaluation was compatible with DKA, and fluids and insulin were given until correction. Because of concerns regarding recurrence of her seizures, the KD was resumed along with the simultaneous use of insulin glargine and insulin aspart. Urine ketones were kept in the moderate range to keep the effect of ketosis on seizure control. Under this combined therapy, the patient remained seizure-free with no new episodes of DKA.
Dietary cholesterol comes exclusively from animal sources, thus it is naturally present in our diet and tissues. It is an important component of cell membranes and a precursor of bile acids, steroid hormones and vitamin D. Contrary to phytosterols (originated from plants), cholesterol is synthesised in the human body in order to maintain a stable pool when dietary intake is low. Given the necessity for cholesterol, very effective intestinal uptake mechanisms and enterohepatic bile acid and cholesterol reabsorption cycles exist; conversely, phytosterols are poorly absorbed and, indeed, rapidly excreted. Dietary cholesterol content does not significantly influence plasma cholesterol values, which are regulated by different genetic and nutritional factors that influence cholesterol absorption or synthesis. Some subjects are hyper-absorbers and others are hyper-responders, which implies new therapeutic issues. Epidemiological data do not support a link between dietary cholesterol and CVD. Recent biological data concerning the effect of dietary cholesterol on LDL receptor-related protein may explain the complexity of the effect of cholesterol on CVD risk.