Literature Review

The effect of (L-)Carnitine on weight loss in adults: A systematic review and meta-analysis of randomized controlled trials

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DOI: 10.1111/obr.12436
Cite this publication
Abstract
This study provides a systematic review and meta-analysis of randomized controlled trials, which have examined the effect of the carnitine on adult weight loss. Relevant studies were identified by systematic search of PubMed, Embase, Cochrane Central Register of Controlled Trials and reference lists of relevant marker studies. Nine studies (total n = 911) of adequate methodological quality were included in the review. Trials with mean difference (MD) of 95% confidence interval (CI) were pooled using random effect model. Results from meta-analysis of eligible trials revealed that subjects who received carnitine lost significantly more weight (MD: -1.33 kg; 95% CI: -2.09 to -0.57) and showed a decrease in body mass index (MD: -0.47 kg m(-2) ; 95% CI: -0.88 to -0.05) compared with the control group. The results of meta-regression analysis of duration of consumption revealed that the magnitude of weight loss resulted by carnitine supplementation significantly decreased over time (p = 0.002). We conclude that receiving the carnitine resulted in weight loss. Using multiple-treatments meta-analysis of the drugs and non-pharmacotherapy options seem to be insightful areas for research. © 2016 World Obesity.
Review
The effect of (L-)carnitine on weight loss in adults: a
systematic review and meta-analysis of randomized
controlled trials
Q1 M. Pooyandjoo,
1
M. Nouhi,
2
S. Shab-Bidar,
3
K. Djafarian
4
and A. Olyaeemanesh
5
1
School of Nutritional Sciences and Dietetics,
Tehran University of Medical Sciences, Tehran,
Iran,
2
Health Management and Economics
Research Center, Iran University of Medical
Sciences, Tehran, Iran,
3
Department of
Community Nutrition, School of Nutritional
Sciences and Dietetics, Tehran University of
Medical Sciences, Tehran, Iran,
4
Department of
Clinical Nutrition, School of Nutritional Sciences
and Dietetics, Tehran University of Medical
Sciences, Tehran, Iran, and
5
National institute
of health research, Tehran University of Medical
Sciences, Tehran, Iran
Received 21 January 2016; revised 21 April
2016; accepted 9 May 2016
Address for correspondence: K Djafarian,
Department of Clinical Nutrition, School of
Nutritional Sciences and Dietetics, Tehran
University of Medical Sciences, Tehran, Iran.
E-mail: kdjafarian@tums.ac.ir
Summary
This study provides a systematic review and meta-analysis of randomized con-
trolled trials, which have examined the effect of the carnitine on adult weight loss.
Relevant studies were identied by systematic search of PubMed, Embase,
Cochrane Central Register of Controlled Trials and reference lists of relevant
marker studies. Nine studies (total n= 911) of adequate methodological quality
were included in the review. Trials with mean difference (MD) of 95% condence
interval (CI) were pooled using random effect model. Results from meta-analysis of
eligible trials revealed that subjects who received carnitine lost signicantly more
weight (MD: 1.33 kg; 95% CI: 2.09 to 0.57) and showed a decrease in body
mass index (MD: 0.47 kg m
2
; 95% CI: 0.88 to 0.05) compared with the con-
trol group. The results of meta-regression analysis of duration of consumption re-
vealed that the magnitude of weight loss resulted by carnitine supplementation
signicantly decreased over time (p= 0.002). We conclude that receiving the carni-
tine resulted in weight loss. Using multiple-treatments meta-analysis of the drugs
and non-pharmacotherapy options seem to be insightful areas for research. ©
2016 World Obesity
Keywords:
Q2 (L-)carnitine, BMI, meta-analysis, placebo, weight change.
obesity reviews (2016)
Introduction
Obesity, an epidemic worldwide issue, can lead to some
chronic diseases such as dyslipidemia (1), type 2 diabetes
mellitus (2), fatty liver (3) and cardiovascular diseases (4).
Pharmacotherapy is a popular approach to weight loss
among individuals. Carnitine is one of the drugs claimed
to increase weight loss.
Carnitine or L-b-hydroxy-c-N-trimethylaminobutyric
acid is synthesized in the liver and kidneys. (L-)carnitine
decreases the intramitochondrial acetyl-CoA/CoA ratio
through trapping of acetyl groups and activation of the
pyruvate dehydrogenase complex (5).
This leads to simultaneous decrease in acetyl-CoA levels
in the cytosol contributing to activation of the glycolytic
pathway (6). (L-)carnitine, thus plays some roles in the
glucose metabolism and may increase energy expenditure
(7,8). Carnitine has an important role in lipid metabolism
as well. It facilitates the transfer of long-chain fatty acids
across the mitochondrial inner membrane as acylcarnitine
esters and acts as an obligatory cofactor for ß-oxidation of
fatty acids (9). Because of these two effects of L-carnitine
obesity reviews doi: 10.1111/obr.12436
© 2016 World Obesity 1
Journal Code Article ID Dispatch: 19.05.16 CE: Belinda Pinili
O B R 12436No.ofPages: 7 ME:
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on glucose and lipid metabolism, it may help weight loss by
increasing energy expenditure (10).
Supplementing carnitine as for weight-loss agent is
based on the fact that regular oral ingestion of this sub-
stance leads to the increase of its intracellular concentra-
tion. This in turn activates fat oxidation and helps
reduction of the bodys fat reserves. A number of studies
have shown that oral carnitine ingestion (up to 6 g d
1
for 14 d) does not change muscle carnitine concentration
in healthy non-obese humans and does not cause weight
loss (11,12). Other clinical studies, however, do report
the effectiveness of carnitine supplementation in the
treatment of obesity (13). A report has revealed that in-
hibition of hypothalamic carnitine palmitoyltransferase
decreases food intake (14). Dietary carnitine stimulates
carnitine palmitoyltransferase activation (15), which
could underlie diminished appetite by L-carnitine supple-
mentation. Thus, claiming that carnitine supplementation
promotes weight loss in healthy non-obese individuals is
not sufciently substantiated, begging more investiga-
tions. Here, we have performed a systematic review and
meta-analysis of randomized clinical trials to evaluate
the effectiveness of L-carnitine supplementation on
weight loss.
Methods
Data source and search strategy
A systematic review and meta-analysis of studies was
conducted based on the Preferred Reporting Items for
Systematic Reviews and Meta-analyses
Q4 guidelines (16).
Comprehensive search strategies were used to identify
reports of randomized controlled trials indexed in PubMed
(from inception to May 2015), the Cochrane Library and
Google scholar (from inception to May 2015). The follow-
ing keywords were used for studies pertinent to the study
objectives: (carnitine OR (L-)carnitine OR Levocarnitine)
AND (weight OR weight loss OR weight reduction OR
BMI OR weight change OR lipid oxidation OR anthropom-
etry) AND (randomized controlled trial OR controlled
clinical trial OR placebo OR randomized OR trial OR
randomly OR group). Moreover, the reference lists of
selected studies were searched to nd other relevant trials.
The language of publication was not restricted.
Study selection
The randomized controlled trial studies comparing the ef-
fects of (L-)carnitine and placebo on the subjectsweight
loss were included. Studies carried out on animals and the
ones with follow-ups of less than 30 d were excluded. (L-)
carnitine is dened as accelerator of fatty acid oxidation in
mitochondria. Placebo was also dened as a medically
ineffectual treatment similar to intervention supplementa-
tion in shape and colour. Weight change was considered as
primary outcome. Other outcomes such as body mass index
(BMI) change and body fat were considered as secondary
outcomes.
Having pooled the retrieved papers and removing dupli-
cates, two reviewers (M. P. and M. N.) independently
skimmed the title and abstracts of searched paper to detect
potentially eligible papers. Then, the body of the selected
studies was scrutinized to exclude non-eligible ones and
include qualied randomized controlled trials reports based
on predetermined criteria. Any discrepancies raised between
reviewers were discussed with a third reviewer (A. O.) in
order to reach a consensus.
Data extraction and quality assessment
A data abstraction form was developed, and the re-
viewers extracted the outcomes of interest from the se-
lected studies. General information (authors, title,
journal of publication and date of publication), the study
population characteristics (age, sex, race, health condi-
tion and BMI) and the study results (predened out-
comes) were extracted. Jadad scale (14) was used to
appraise the included studies. Randomization allocation,
allocation concealment and blinding of outcome assess-
ment were some of the criteria.
Qualitative and quantitative analysis
Mean difference (MD) was used as the main measure to
summarize clinical effect of the arms on the outcomes.
Inverse-variance method was used to analyze the prepared
data. To calculate pooled estimate of MD with 95% con-
dence interval (CI), the xed effects and random effects
models were used. I
2
test was used to assess heterogeneity.
I
2
>50% was assumed to represent heterogeneity among
studies. If heterogeneity of the studies was not signicant,
the xed effects estimation was reported. Sensitivity analysis
of results was used to explore heterogeneity among trials.
Meta-analysis was performed using REVMAN 5.2 software
and meta-regression analysis was performed using STATA
14 software.
Results
A total of 2,145 studies were retrieved through search data-
bases as depicted in Fig. F11. Having excluded the duplicates,
the summaries of the 1,236 remaining studies were screened
by the reviewers. Next, the body of the remaining 83 studies
were scrutinized. At the end, nine studies were included in
the review. Four of the studies had been conducted in Italy
(1821), and two in Iran (22,23). The other trials had been
conducted in New Zealand (24), Australia (25) and Brazil
(26). Of the total 911 individuals participated in the
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included trials, 449 had received carnitine, and the remain-
ing 462 subjects had been allocated to placebo/control arm.
The publication year of included trials ranged from 2000 to
2013, spanning 13 years.
Moreover, four trials had compared (L-)carnitine with
placebo (18,19,24,26). However, in the comparative arms
of some studies, the subjects of both arms also had followed
exercise protocol (12,23) or some complementary drugs
(20,21). Four studies had included diabetic patients
(18,2022). One study had been conducted on subjects with
bipolar disorder (24), and two studies had investigated
obese subjects (12,23). One study had focused on physically
active individuals (26), and the last trial had included sub-
jects with muscle fatigue (19). Table T11 summarizes charac-
teristics of the included trials.
Assessment the quality of studies
All of the included studies had adopted randomization
criteria but some of them did not delineate clearly the
schedule of randomization process (12,22,26). The
blinding had been conducted in all of the included stud-
ies except for two studies (22,26). According to the
Jadad scale, ve studies received score 5
(18,20,21,23,24). Last column of Table 1 provides
detailed results of quality assessment of the studies.
Figure 1 Flowchart of identication of included trials.
Table 1 Characteristics of included studies
Author Year Population Arms (dosage)
Sample size
(women %) Mean age (SD) Baseline weight
Follow-up
duration (day)
Quality
assessment
Barzegar
et al.
2013 Diabetic obese
women
(L-)carnitine (2 g d
1
)
and low calorie diet
30 (0) Range from
20 to 50
83.8 (8.21) 56 1
Placebo and low calorie diet 30 (0) 84.23 (7.8)
Coelho
et al.
2009 Physically active
individuals
(L-)carnitine (1.8 g d
1
) 11 (0) 46.7 (4.8) 82.35 (16.36) 30 2
Placebo 10 (0) 44.7 (5) 83.57 (14.35)
Derosa
et al.
2003 Diabetic patients (L-)carnitine (2 g d
1
) 46 (47.8) 52 (6) 78.2 (5.8) 90 5
Placebo 48 (52.1) 50 (7) 77.6 (6.4)
Derosa
et al.
2010 Obese diabetic
patients
(L-)carnitine (2 g d
1
)
and orlistat
132 (50.7) 51 (4) 94.5 (9.6) 360 5
Orlistat 126 (50.7) 53 (6)
Derosa
et al.
2011 Diabetic patients (L-)carnitine (2 g d
1
) and
sibutramine (10 mg)
129 (49.6) 54 (5) 97.7 (11.4) 360 5
sibutramine (10 mg) 125 (49.6) 51 (4) 96.9 (10.8)
Elmslie
et al.
2006 Patients with
bipolar disorder
(L-)carnitine (15 mg kg
1
d
1
) 30 (20) 42 (10) 94.7 182 5
Placebo 30 (16.6) 42 (13) 94.1
Pistone
et al.
2003 Elderly patients Levocarnitine (4 g d
1
) 42 (47.6) 81.5 (6.7) 66.9 (9.4) 30 4
Placebo 42 (42.9) 80.7 (6.9) 65.4 (11.3)
Rafraf 2012 Diabetic women (L-)carnitin e (2 g d
1
) 11 (100) 34.4 (5.48) 87.72 (6.31) 60 5
(L-)carnitine (2 g d
1
)
and exercise
11 (100) 34.8 (6.25) 85.08 (11.65)
Placebo 11 (100) 36.5 (7.33) 85.6 (8.87)
Placebo and exercise 11 (100) 36.1 (7.2) 82.61 (6.06)
Vilani
et al.
2000 Obese women (L-)carnitine (4 g d
1
) and
aerobic training programme
18 (100) 27.2 (9.6) 70.1 (9.9) 56 3
Placebo and aerobic training
programme
18 (100)
SD, standard deviation.
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Data synthesis
Nine trials were included in this review, but only six of them
had reported the mean (standard deviation) of weight and ve
of them had reported mean (standard deviation) of BMI. One
trial was excluded from meta-analysis because of reporting
ndings with median and two of the remaining trials did not
report neither BMI or weight outcomes properly.
The eligible trials for quantitative analysis had reported
their ndings in different time points and with no estimation
of changes in weight or BMI outcomes. Some reviews had
used different implicit methods to determine the effect of the
treatment (27,28). The steps followed in this study are clearly
dened in the Tables S1S4. This method had been used in dif-
ferent review studies (29,30). The subgroup analysis was con-
sidered for some chronic conditions such as diabetes and
obesity. Insufcient available data on other potential causes
of heterogeneities such as age and gender of subjects hinder
an assessment of subgroup differences in the included trials.
Weight change
Six trials had reported weight changes in control and inter-
vention groups. Using inverse-variance method, a signi-
cantly greater loss in weight was observed in participants
who received the carnitine compared with control group,
(MD: 1.33 kg; 95% CI: 2.09 to 0.57) I
2
= 96%.
FigureF2 2 represents the forest plot of these results.
Body mass index change
Five trials had used this outcome to report their ndings. Our
analysis indicates that using the carnitine leads to signicantly
lower BMI compared with subjects who had received control,
(MD: 0.47 kg m
2
;95%CI:0.88 to 0.05) I
2
=93%.
Figure F33 represents the forest plot of these results.
Subgroup and meta-regression analysis
Diabetic versus non-diabetic patients
Three trials had been conducted on patients suffering from di-
abetes. Pool estimate of their results indicated that those who
received carnitine had signicantly much weight loss com-
pared with control group, (MD: 1.96kg; 95% CI: 2.21
to 1.7) I
2
= 0%. In non-diabetic people a signicant weight
loss was observed, (MD: 0.54 kg; 95% CI: 0.6 to 0.49)
I
2
= 0%. Figure F44 show the forest plot of this analysis.
Obese versus non-obese participants
Totally, ve trials involved obese subjects. Our results show
that those who had received carnitine experienced a signi-
cantly much weight loss compared with the control group,
(MD: 1.25 kg; 95% CI: 2.14 to 0.36) I
2
= 97%. In
non-obese as well- a signicant weight loss was observed,
(MD: 1.75 kg; 95% CI: 2.37 to 1.12) I
2
= 0%.
Figure F55 represents the forest plot of this analysis.
Dosage and duration of consumption
Duration of the trials included varied from1-month to 1-year
follow-up.Meta-regression analysis showed that the duration
of consumption were negatively related to effect size (regres-
sion coefcient = 0.24; 95% CI: 0.38, 0.09 p=0.002).
It means when the carnitine was used for longer time, it ex-
pected that the magnitude of weight loss will decrease.
Figure 2 Forest plot of weight change outcome.
Figure 3 Forest plot of body mass index (BMI) change outcome.
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The carnitine dosage varies from 1.8 g d
1
to 4 g d
1
in the
trials. Meta-regression analysis done emphasized that dose of
the carnitine did not signicantly change the effect size (regres-
sion coefcient = 0.06; 95% CI: 3.16, 3.28 p=0.972).
Sensitivity analysis
Regarding the considerable heterogeneity among the included
trials, it was found that most heterogenic trials in pool estima-
tion of the outcomes were related to those studies that had
low score in methodological quality assessment such as
Villani et al. (12) and Barzegar et al. (22). However, the sensi-
tivity analysis of these trials did not affect our nal results.
Discussion
Obesity is a serious health problem, which has increasingly be-
come associated with higher rate of mortality and morbidity in
the world. Along with weight control as becoming more
difcult in this industrialized world, weight loss is getting more
attention. Anti-obesity drugs have no side effects of invasive
surgeries, and hence, they are more commonly used than other
options like physical activities. Carnitine has been applied for
prevention of cardiovascular disease (31), end-stage kidney dis-
eases (32), dialysis-related hypertension (33), treatment of per-
sistent depressive disorder (34) and treatment of non-alcoholic
fatty liver disease (35). However, evidence regarding the anti-
obesity effects of the carnitine is still inconclusive. Here, we
pooled the trials comparing the effect of carnitine and control
on weight loss in adults. Weight and BMI were two variables
that were considered as for assessing weight loss of the partic-
ipants. After, excluding the studies that did not meet our
criteria, nine studies were accepted for nal analysis. However,
only seven of them were eligible for quantitative analysis. Most
of the included trials were of relatively adequate methodologi-
cal quality. We found that carnitine has had a decreasing im-
pact onto weight and BMI in these trials. Positive inuence of
carnitine onto weight loss was found in chronic conditions
such as diabetes and obesity. Our meta-regression analysis
Figure 4 Forest plot of diabetic patents.
Figure 5 Forest plot of obese people.
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indicates that magnitude of weight loss would decrease over
time. Although the analysis indicated that dosage of carnitine
had positive, but not signicant, impact on weight change, in-
sufcient power of analysis precluded us to have any recom-
mendation regarding the best dosage of the carnitine. No
study had systematically reviewed anti-obesity impact of the
carnitine. There was, however, a narrative review, which had
focused on metabolic function of the carnitine in human setting
(36), but that study has not directly addressed clinical effect of
carnitine. Evidence about pharmacotherapy of obesity have
addressed the long-term impact of orlistat, sibutramine and
rimonabant on weight loss in people (37,38). Although carni-
tine has a lower magnitude of weight loss than these drugs, un-
like them, it does not suffer from some side-effects such as
gastrointestinal issues, rising blood pressure, and pulse rate
and increased risk of psychological disorder (39,40). The re-
searchers had some trials, which had relatively heterogenic
characteristics. Lack of sufcient data precluded us to assess
the impact of the variables on effect size of the study. More in-
vestigations would help to have a better assessment of the com-
parative effect of the anti-obesity drugs in long-term follow-up
studies. Multiple-treatments meta-analysis of the drugs and
non-pharmacotherapy options might be helpful in this regard.
Conclusions
Carnitine might be an effective drug for weight loss in
adults.
Conict of interest statement
The authors declared that they have no potential conicts of
interest.
Acknowledgements
This review was funded by Tehran University of Medical
Sciences. We thank the referees for their valuable comments.
Supporting Information
Additional Supporting Information may be found in the
online version of this article, http://dx.doi.org/10.1111/
obr.12436
References
1. Fried M, Hainer V, Basdevant A et al. Interdisciplinary
European guidelines on surgery of severe obesity. Obes Facts
2008; 1:5259.
2. Pagotto U, Vanuzzo D, Vicennati V, Pasquali R. Pharmacologi-
cal therapy of obesity. G Ita Cardiol 2008; 9: 83S93S.
3. MarovićD. Elevated body mass index and fatty liver. Srp Arh
Celok Lek 2008; 136: 12225.
4. Artham SM, Lavie CJ, Milani RV, Ventura HO. The obesity
paradox: impact of obesity on the prevalence and prognosis of
cardiovascular diseases. Postgrad Med 2008; 120:3441.
5. Uziel G, Garavaglia B, Di Donato S. Carnitine stimulation of
pyruvate dehydrogenase complex (PDHC) in isolated human
skeletal muscle mitochondria. Muscle Nerve 1988; 11: 72024.
6. di San Filippo CA, Taylor MR, Mestroni L, Botto LD, Longo N.
Cardiomyopathy and carnitine deciency. Mol Gen Metab 2008;
94: 16266.
7. Kim JH, Pan JH, Lee ES, Kim YJ. L-carnitine enhances exercise
endurance capacity by promoting muscle oxidative metabolism in
mice. Biochem Biophys Res Commun 2015; 464: 56873.
8. Wall BT, Stephens FB, Constantin-Teodosiu D, Marimuthu K,
Macdonald IA, Greenhaff PL. Chronic oral ingestion of L-carnitine
and carbohydrate increases muscle carnitine content and alters
muscle fuel metabolism during exercise in humans. J Physiol
2011; 589: 96373.
9. Torgerson JS, Hauptman J, Boldrin MN, Sjöström L. XENical
in the Prevention of Diabetes in Obese Subjects (XENDOS) Study:
a randomized study of orlistat as an adjunct to lifestyle changes
for the prevention of type 2 diabetes in obese patients. Diabetes
Care 2004; 27: 15561.
10. Jeukendrup A, Randell R. Fat burners: nutrition supplements
that increase fat metabolism. Obes Rev 2011; 12: 84151.
11. Barnett C, Costill DL, Vukovich MD et al. Effect of L-carnitine
supplementation on muscle and blood carnitine content and lactate
accumulation during high-intensity sprint cycling. Int J Sport Nutr
Exerc Metab 1994; 4: 28088.
12. Villani RG, Gannon J, Self M, Rich PA. L-carnitine supplemen-
tation combined with aerobic training does not promote weight loss
in moderately obese women. Int J Sport Nutr Exerc Metab 2000;
10: 199207.
13. Walter P, Schaffhauser AO. L-carnitine, a vitamin-like
substancefor functional food. Proceedings of the symposium on
L-carnitine, April 28 to May 1, 2000, Zermatt, Switzerland. Ann
Nutr Metab 2000; 44:7596.
14. Obici S, Feng Z, Arduini A, Conti R, Rossetti L. Inhibition of
hypothalamic carnitine palmitoyltransferase-1 decreases food
intake and glucose production. Nat Med 2003; 9: 75661.
15. Karlic H, Lohninger S, Koeck T, Lohninger A. Dietary
L-carnitine stimulates carnitine acyltransferases in the liver of aged
rats. J Histochem Cytochem 2002; 50: 20512.
16. Moher D, Liberati A, Tetzlaff J, Altman DG. Preferred
reporting items for systematic reviews and meta-analyses: the
PRISMA statement. PLoS Med 2009; 6: e1000097.
17. Q5Jadad AR, Moore RA, Carroll D et al. Assessing the quality of
reports of randomized clinical trials: is blinding necessary? Control
Clin Trials 1996; 17:112.
18. Derosa G, Cicero AF, Gaddi A, Mugellini A, Ciccarelli L,
Fogari R. The effect of L-carnitine on plasma lipoprotein(a) levels
in hypercholesterolemic patients with type 2 diabetes mellitus. Clin
Ther 2003; 25: 142939.
19. Pistone G, Marino A, Leotta C, DellArte S, Finocchiaro G,
Malaguarnera M. Levocarnitine administration in elderly subjects
with rapid muscle fatigue: effect on body composition, lipid prole
and fatigue. Drug & Aging 2003; 20: 7617.
20. Derosa G, Mafoli P, Salvadeo SA et al. Comparison of orlistat
treatment and placebo in obese type 2 diabetic patients. Expert
Opin Pharmacother 2010; 11: 197182.
21. Derosa G, Mafoli P, Salvadeo SA et al. Effects of combination
of sibutramine and L-carnitine compared with sibutramine
monotherapy on inammatory parameters in diabetic patients.
Metabolism 2011; 60: 4219.
22. Barzegar A, Alipour B, Panahi F, Karamzad N. Effect of
L-carnitine supplementation on serum adipokines (leptin and
6Carnitine and weight loss M. Pooyandjoo et al. obesity reviews
© 2016 World Obesity
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visfatin) levels in obese type II diabetes mellitus women with
hypocaloric diet. Life Sci J 2013; 10: 35965.
23. Rafraf M, Karimi M, Rashidi M, Jafari A. Effect of L-carnitine
supplementation in comparison with moderate aerobic training on
insulin resistance and anthropometric indices in obese women. Sci
J Zanjan Univ Med Univ 2012; 20:1730.
24. Elmslie JL, Porter RJ, Joyce PR, Hunt PJ, Mann JI. Carnitine
does not improve weight loss outcomes in valproate-treated bipolar
patients consuming an energy-restricted, low-fat diet. Bipolar
Disord 2005; 8: 50307.
25. Villani RG, Gannon J, Self M, Rich PA. L-carnitine supplemen-
tation combined with aerobic training does not promote weight loss
in moderately obese women. Int J Sport Nutr Exerc Metab 2000;
10: 199207.
26. Coelho CF, Mota JF, Ravagnani FCP, Burini RC. The supple-
mentation of L-carnitine does not promote alterations in the resting
metabolic rate and in the use of energetic substrates in physically
active individuals. Arq Bras Endocrinol Metab 2009; 54:3744.
27. Brunoni AR, Lopes M, Fregni F. A systematic review and meta-
analysis of clinical studies on major depression and BDNF levels:
implications for the role of neuroplasticity in depression. Int J
Neuropsychopharmacol 2008; 11: 116980.
28. Agerholm-Larsen L, Bell M, Grunwald G, Astrup A. The effect of
a probiotic milk product on plasma cholesterol: a meta-analysis of
short-term intervention studies. Eur J Clin Nutr 2000; 54:85660.
29. Dansinger ML, Tatsioni A, Wong JB, Chung M, Balk EM.
Meta-analysis: the effect of dietary counseling for weight loss.
Ann Intern Med 2007; 147:4150.
30. Ballantyne JC, Carr DB, Suarez Tet al. The comparative effects
of postoperative analgesic therapies on pulmonary outcome:
cumulative meta-analyses of randomized, controlled trials. Anesth
Analg 1998; 86: 598612.
31. Shang R, Sun Z, Li H. Effective dosing of L-carnitine in the
secondary prevention of cardiovascular disease: a systematic review
and meta-analysis. BMC Cardiovasc Disord 2014; 14: 88.
32. Chen Y, Abbate M, Tang L et al. L-carnitine supplementation
for adults with end-stage kidney disease requiring maintenance
hemodialysis: a systematic review and meta-analysis. Am J Clin
Nutr 2014; 99: 40822.
33. Lynch KE, Feldman HI, Berlin JA, Flory J, Rowan CG, Brunelli
SM. Effects of L-carnitine on dialysis-related hypotension and mus-
cle cramps: a meta-analysis. Am J Kidney Dis 2008; 52: 96271.
34. Kriston L, Wolff A, Westphal A, Hölzel LP, Härter M. Efcacy
and acceptability of acute treatments for persistent depressive disor-
der: a network meta-analysis. Depress Anxiety 2014; 31: 62130.
35. Musso G, Gambino R, Cassader M, Pagano G. A meta-analysis
of randomized trials for the treatment of nonalcoholic fatty liver
disease. Hepatology 2010; 52:79104.
36. Pekala J, Patkowska-Sokola B, Bodkowski R et al. L-carnitine-
metabolic functions and meaning in humans life. Curr Drug Metab
2011; 12: 66778.
37. Rueda-Clausen CF, Padwal RS. Pharmacotherapy for weight
loss. 2014.
38. Padwal RS, Majumdar SR. Drug treatments for obesity:
orlistat, sibutramine, and rimonabant. Lancet 2007; 369:7177.
39. Rucker D, Padwal R, Li SK, Curioni C, Lau DC. Long-term
pharmacotherapy for obesity and overweight: updated
meta-analysis. BMJ 2007; 335: 119499.
40. Padwal R, Li S, Lau D. Long-term pharmacotherapy for
obesity and overweight. Cochrane Database Syst Rev 2003; (4). Q6
Carnitine and weight loss M. Pooyandjoo et al. 7obesity reviews
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  • ... Experiments using 13 CO2 exhalation gas analysis with 13 C-labeled long-chain fatty acid probes showed that 10 d of supplementation with 3 g/d l-carnitine significantly promoted b-oxidation of exogenously ingested fatty acids (4,5). Pooyandjoo et al. performed a systematic review with a meta-analysis of nine studies on the effects of oral lcarnitine intake on weight management and concluded that the supplementation resulted in significant weight loss (6), which meant that exogenous l-carnitine worked for the consumption of stored body fat. In the clinical trials evaluated in this systematic review, the duration of supplementation was 30-360 d with a dosage level of 1.8-4 g/d. ...
    Article
    The acute metabolic effect of low dosages of L-carnitine under fat-mobilizing conditions was investigated. Healthy subjects (Study 1: n=5; Study 2: n=6) were asked to fast overnight. Then, 30 min of aerobic exercise on a cycle ergometer was performed after supplementation, followed by a 3.5-h sedentary recovery phase. The following ingestion patterns were used: Study 1 (i) noningestion, (ii) 750 mg of L-carnitine (LC), and (iii) 750 mg of LC+50 g of carbohydrate (CHO); Study 2 (iv) noningestion, (v) 500 mg of LC, (vi) 30 mg of CoQ10, and (vii) 500 mg of LC+30 mg of CoQ10. The energy expenditure (EE) and nonprotein respiratory quotient (npRQ) were measured during the pre-exercise, postexercise, and recovery periods. Serum free carnitine, acetylcarnitine, total carnitine (Study 1 and 2), and ketone bodies (Study 2) were measured. The 750 mg LC treatment significantly facilitated fat oxidation during the recovery phases (p<0.05) without elevating EE. The higher fat oxidation associated with LC was completely suppressed by CHO. CoQ10 affected neither npRQ nor EE. npRQ was significantly correlated with the serum total ketone bodies (R=−0.68, p<0.001) and acetylcarnitine (R=−0.61-−0.70, p<0.001). The highest correlation was found between acetylcarnitine and total ketone bodies immediately after exercise (R=0.85, p<0.001). In conclusion, LC enhanced liver fat utilization and ketogenesis in an acute manner without stimulating EE under fat-mobilizing conditions.
  • ... Therefore, early and efficient intervention increases likelihood of staying healthy in the future. As pharmacological and surgical interventions in children are limited [15][16][17], trials looking for substances supporting lifestyle interventions were run, looking at several different dietary supplements, hers (green tea, yerba mate), DHA (docosahexaenoic acid) among others [18][19][20][21][22]. Vitamin D was also studied in regards to its possible impact on body mass reduction and metabolic changes in adults and children with obesity [23,24]. ...
    Article
    Full-text available
    Background: Vitamin D was studied in regards to its possible impact on body mass reduction and metabolic changes in adults and children with obesity yet there were no studies assessing the impact of vitamin D supplementation during a weight management program in children and adolescence. The aim of our study was to assess the influence of 26 weeks of vitamin D supplementation in overweight and obese children undergoing an integrated 12-months' long weight loss program on body mass reduction, body composition and bone mineral density. Methods: A double-blind randomized placebo-controlled trial. Vitamin D deficient patients (<30 ng/ml level of vitamin D) aged 6-14, participating in multidisciplinary weight management program were randomly allocated to receiving vitamin D (1200 IU) or placebo for the first 26 weeks of the intervention. Results: Out of the 152 qualified patients, 109 (72%) completed a full cycle of four visits scheduled in the program. There were no difference in the level of BMI (body mass index) change - both raw BMI and BMI centiles. Although the reduction of BMI centiles was greater in the vitamin D vs. placebo group (-4.28 ± 8.43 vs. -2.53 ± 6.10) the difference was not statistically significant (p = 0.319). Similarly the reduction in fat mass-assessed both using bioimpedance and DEXa was achieved, yet the differences between the groups were not statistically significant. Conclusions: Our study ads substantial results to support the thesis on no effect of vitamin D supplementation on body weight reduction in children and adolescents with vitamin D insufficiency undergoing a weight management program.
  • ... Therefore, early and efficient intervention increases likelihood of staying healthy in the future. As pharmacological and surgical interventions in children are limited [15][16][17], trials looking for substances supporting lifestyle interventions were run, looking at several different dietary supplements, hers (green tea, yerba mate), DHA among others [18][19][20][21][22]. Vitamin D was also studied in regards to its possible impact on body mass reduction and metabolic changes in adults and children with obesity [23,24]. ...
    Preprint
    Background: Vitamin D was studied in regards to its possible impact on body mass reduction and metabolic changes in adults and children with obesity yet there were no studies assessing the impact of vitamin D supplementation during a weight management programme in children and adolescence. The aim of our study was to assess the influence of 26 weeks of vitamin D supplementation in overweight and obese children undergoing an integrated 12-months' long weight loss programme on body mass reduction, body composition and bone mineral density. Mathods: A double-blind randomized placebo-controlled trial. Vitamin D deficient patients (<30 ng/ml level of vitamin D) aged 6-14, participating in multidisciplinary weight management programme were randomly allocated to receiving vitamin D (1200 IU) or placebo for the first 26 weeks of the intervention. Results: Out of the 152 qualified patients, 109 (72%) completed a full cycle of four visits scheduled in the programme. There were no difference in the level of BMI change. Although the reduction was greater in the vitamin D vs. placebo group (-4.28 ± 8.43 vs.-2.53 ±6.10) the difference was not statistically significant (p=0.319). Similarly the reduction in fat mass-assessed both using bioimpedance and DEXa was achieved, yet the differences between the groups were not statistically significant. Conclusions: Our study ads substantial results to support the thesis on no effect of vitamin D supplementation on body weight reduction in children and adolescents with vitamin D insufficiency undergoing a weight management programme. Trial registration no: NCT 02828228; trial registration date: 8 June 2016 registered in: ClinicalTrials.gov.
  • ... In a further meta-analysis of ten RCT enrolling 925 patients, L-carnitine consumption was associated with significant reductions in serum CRP (-0·60 mg/l (5·71 nmol/l); 95 % CI -0·87, -0·32 mg/l) and TNF-α concentrations (-0·36 (95 % CI -0·56, -0·15) pg/ml) (76) . Then, L-carnitine supplementation could have a mild but significant impact on body weight (77) and plasma level of lipoprotein (a) (78) . The prognostic importance and clinical relevance of these data still need to be clarified (Table 2). ...
    Article
    Heart failure (HF) is a complex clinical syndrome that represents a major cause of morbidity and mortality in Western countries. Several nutraceuticals have shown interesting clinical results in HF prevention as well as in the treatment of the early stages of the disease, alone or in combination with pharmacological therapy. The aim of the present expert opinion position paper is to summarise the available clinical evidence on the role of phytochemicals in HF prevention and/or treatment that might be considered in those patients not treated optimally as well as in those with low therapy adherence. The level of evidence and the strength of recommendation of particular HF treatment options were weighed up and graded according to predefined scales. A systematic search strategy was developed to identify trials in PubMed (January 1970 to June 2019). The terms 'nutraceuticals', 'dietary supplements', 'herbal drug' and 'heart failure' or 'left verntricular dysfunction' were used in the literature search. The experts discussed and agreed on the recommendation levels. Available clinical trials reported that the intake of some nutraceuticals (hawthorn, coenzyme Q 10 , L-carnitine, D-ribose, carnosine, vitamin D, probiotics, n-3 PUFA and beet nitrates) might Abbreviations: 25(OH)D, 25-hydroxyvitamin D; 6MWT, 6-min walking test; AA, amino acid; BNP, brain natriuretic peptide be associated with improvements in self-perceived quality of life and/or functional parameters such as left ventricular ejection fraction, stroke volume and cardiac output in HF patients, with minimal or no side effects. Those benefits tended to be greater in earlier HF stages. Available clinical evidence supports the usefulness of supplementation with some nutraceuticals to improve HF management in addition to evidence-based pharmacological therapy.
  • ... Despite common use of L-carnitine as diet supplement routinely used for building of muscle mass and muscular strength and also as fat tissue burning [3] its regulatory effects are poorly understood. L-carnitine was reported to improve systolic function of the left ventricle in patients with heart failure [11], after acute myocardial infarction [12], reduce inflammation and fibrosis in coronary heart disease [13], improve cardiac electrophysiological parameters, ameliorate peripheral neuropathy in diabetes [14], improve body weight reduction during obesity treatment [15], and many more. L-carnitine, by its contribution in the transport of fatty acids through mitochondrial membrane, was thought not only to improve skeletal muscle and cardiac function in older people but also to support ANS regulatory control. ...
  • ... Notably, contradictive results were present regarding to L-carnitine's effects on obesity and metabolic syndrome. While it is generally accepted that L-carnitine supplement is not effective in weight loss or correcting dyslipidemia [16], evidences supporting its effect on obesity and improving lipid metabolism were also reported [17,18]. It is necessary to further investigate the role of L-carnitine in fatty acid metabolism dysfunction. ...
    Article
    Full-text available
    Lipid metabolism dysfunction and obesity are serious health issues to human beings. The current study investigated the effects of hyperbaric oxygen (HBO) against high fat diet (HFD)-induced lipid metabolism dysfunction and the roles of L-carnitine. C57/B6 mice were fed with HFD or normal chew diet, with or without HBO treatment. Histopathological methods were used to assess the adipose tissues, serum free fatty acid (FFA) levels were assessed with enzymatic methods, and the endogenous circulation and skeletal muscle L-carnitine levels were assessed with liquid chromatography-tandem mass spectrometry (LC-MS/MS). Additionally, western blotting was used to assess the expression levels of PPARα, CPT1b, pHSL/HSL, and UCP1. HFD treatment increased body/adipose tissue weight, serum FFA levels, circulation L-carnitines and decreased skeletal muscle L-carnitine levels, while HBO treatment alleviated such changes. Moreover, HFD treatment increased fatty acid deposition in adipose tissues and decreased the expression of HSL, while HBO treatment alleviated such changes. Additionally, HFD treatment decreased the expression levels of PPARα and increased those of CPT1b in skeletal muscle, while HBO treatment effectively reverted such changes as well. In brown adipose tissues, HFD increased the expression of UCP1 and the phosphorylation of HSL, which was abolished by HBO treatment as well. In summary, HBO treatment may alleviate HFD-induced fatty acid metabolism dysfunction in C57/B6 mice, which seems to be associated with circulation and skeletal muscle L-carnitine levels and PPARα expression.
  • ... Due to the availability of carnitine over-the-counter, the use of carnitine as a supplement is often disproportionate among endurance athletes. Furthermore, since it has been suggested that carnitine saves muscle glycogen and promotes fat oxidation [69], its integration is recommended to lose weight. Carnitine supplementation has been also reported to spare the use of amino acids as energy sources during exercise making them potentially available for new protein synthesis [70]. ...
    Article
    Full-text available
    l-Carnitine is an amino acid derivative widely known for its involvement in the transport of long-chain fatty acids into the mitochondrial matrix, where fatty acid oxidation occurs. Moreover, l-Carnitine protects the cell from acyl-CoA accretion through the generation of acylcarnitines. Circulating carnitine is mainly supplied by animal-based food products and to a lesser extent by endogenous biosynthesis in the liver and kidney. Human muscle contains high amounts of carnitine but it depends on the uptake of this compound from the bloodstream, due to muscle inability to synthesize carnitine. Mitochondrial fatty acid oxidation represents an important energy source for muscle metabolism particularly during physical exercise. However, especially during high-intensity exercise, this process seems to be limited by the mitochondrial availability of free l-carnitine. Hence, fatty acid oxidation rapidly declines, increasing exercise intensity from moderate to high. Considering the important role of fatty acids in muscle bioenergetics, and the limiting effect of free carnitine in fatty acid oxidation during endurance exercise, l-carnitine supplementation has been hypothesized to improve exercise performance. So far, the question of the role of l-carnitine supplementation on muscle performance has not definitively been clarified. Differences in exercise intensity, training or conditioning of the subjects, amount of l-carnitine administered, route and timing of administration relative to the exercise led to different experimental results. In this review, we will describe the role of l-carnitine in muscle energetics and the main causes that led to conflicting data on the use of l-carnitine as a supplement.
  • ... Second, this bound fat still needs to leave the body, which it often does in the form of stomach pain, unpleasant anal leakage, and diarrhea. Chitosan is recommended for reducing lowering cholesterol levels and promoting weight loss (Pooyandjoo et al. 2016;Vincent et al. 2003). ...
    Article
    Full-text available
    Adipose tissue is a type of connective tissue composed of adipocytes. Recently, this tissue has been recognized as a major endocrine organ. The physiological process of fat loss occurs when fats are liberated from adipocytes into circulation to supply the needed energy. Nutrition supplements that increase fat metabolism, impair fat absorption, increase weight loss, and increase fat oxidation during exercise are known as fat burners. A good fat burner must burn the stored fats, break down the fat cells, and increase the metabolic rate. Eating thermogenic foods helps burn fats. Fat flush diet comes to repair the damage that resulted from ingested and environmental toxins stored in adipocytes. This review will focus on the recent advances in fat burning supplements, fat burning foods, and fat flash diet. The human body can act as a fat-burning machine by depending on low-calorie foods instead of high-calorie foods in addition to doing regular exercise, avoiding toxins and processed food, and applying any fat flush dietary program under the approval of a professional doctor. What’s new in this review is that it may orient our attention to the importance of using natural fat burners in the fat burning process in an attempt to avoid medications that have many side effects by targeting other organs and it also gives an idea of the importance of increasing the brown adipose tissue content because its activation could be linked to a feeling of being full. We need further studies in this context.
  • Chapter
    Vegetables are the major protective food in our diet, and besides providing essential nutrients, they are also the reservoirs of bioactive compounds. Bioactive compounds are the secondary metabolites that have an effect on living organisms and impart many health benefits. Most prominent bioactive compounds present in vegetables are terpenoids, carotenoids, phenolics, phytosterols, and glucosinolates. Many of these bioactive compounds are reported to possess antioxidant, immunomodulatory, anti-osteoporotic, antihypertensive, antimicrobial, antidiabetic, and anticancer properties, and are said to be effective as the reducers of cardiovascular complications. These bioactives can be extracted by various extraction techniques, and the extracted bioactives are evaluated using multiple in vitro and in vivo methods to ascertain their health benefits. This book chapter summarizes the literature available on bioactive compounds present in vegetables along with their health benefits, their extraction methods and effect of storage and processing on bioactive constituent retention.
Literature Review
  • Article
    Background and Objective: Insulin resistance is one of the key components of metabolic syndrome and a major risk factor for diabetes and cardio-vascular diseases, especially among obese people. The aim of this study was to evaluate the effects of L-carnitine supplementation either with or without moderate aerobic training on insulin resistance and anthropometric indices in obese women. Materials and Methods: In this clinical trial, 44 obese women (BMI≥30 kg/m2) were randomly assigned into 4 groups (n=11 each) as follows: 1, L-carnitine supplementation (2 g/day) (group CAR); 2, aerobic training + placebo (group EXR+PLA); 3, L-carnitine supplementation + aerobic training (group CAR+EXR); and 4, placebo alone (group PLA). The intervention periods were eight-week long, and the subjects of aerobic training groups went through 3 training sessions a week. The weight, waist and hip circumferences, waist to hip ratios, body mass indeces, daily dietary intakes and serum fasting free L-carnitine levels, glucose and insulin levels, and HOMA-IR were measured before and after the interventions. Results: Significant decreases in the waist and hip circumferences were observed in the EXR+PLA and CAR+EXR groups. The serum glucose fasting levels, as well as insulin and HOMA-IR (homeostasis model assessment-estimated insulin resistance) values decreased significantly in the CAR, EXR+PLA, and CAR+EXR groups. Conclusion: The results indicate beneficial effect of aerobic training on insulin resistance and anthropometric measurements including waist and hip circumferences in comparison with L-carnitine alone supplementation. L-carnitine decreased the insulin resistance and was more effective along with aerobic training for improvement of insulin resistance. The aerobic training could be considered as an effective way of weight loss and insulin resistance improvement.
  • Article
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    Systematic reviews should build on a protocol that describes the rationale, hypothesis, and planned methods of the review; few reviews report whether a protocol exists. Detailed, well-described protocols can facilitate the understanding and appraisal of the review methods, as well as the detection of modifications to methods and selective reporting in completed reviews. We describe the development of a reporting guideline, the Preferred Reporting Items for Systematic reviews and Meta-Analyses for Protocols 2015 (PRISMA-P 2015). PRISMA-P consists of a 17-item checklist intended to facilitate the preparation and reporting of a robust protocol for the systematic review. Funders and those commissioning reviews might consider mandating the use of the checklist to facilitate the submission of relevant protocol information in funding applications. Similarly, peer reviewers and editors can use the guidance to gauge the completeness and transparency of a systematic review protocol submitted for publication in a journal or other medium.
  • Article
    We performed meta-analyses of randomized, control trials to assess the effects of seven analgesic therapies on postoperative pulmonary function after a variety of procedures: epidural opioid, epidural local anesthetic, epidural opioid with local anesthetic, thoracic versus lumbar epidural opioid, intercostal nerve block, wound infiltration with local anesthetic, and intrapleural local anesthetic. Measures of forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), vital capacity (VC), peak expiratory flow rate (PEFR), PaO2, and incidence of atelectasis, pulmonary infection, and pulmonary complications overall were analyzed. Compared with systemic opioids, epidural opioids decreased the incidence of atelectasis (risk ratio [RR] 0.53, 95% confidence interval [CI] 0.33-0.85) and had a weak tendency to reduce the incidence of pulmonary infections (RR 0.53, 95% CI 0.18-1.53) and pulmonary complications overall (RR 0.51, 95% CI 0.20-1.33). Epidural local anesthetics increased PaO2 (difference 4.56 mm Hg, 95% CI 0.058-9.075) and decreased the incidence of pulmonary infections (RR 0.36, 95% CI 0.21-0.65) and pulmonary complications overall (RR 0.58, 95% CI 0.42-0.80) compared with systemic opioids. Intercostal nerve blockade tends to improve pulmonary outcome measures (incidence of atelectasis: RR 0.65, 95% CI 0.27-1.57, incidence of pulmonary complications overall: RR 0.47, 95% CI 0.18-1.22), but these differences did not achieve statistical significance. There were no clinically or statistically significant differences in the surrogate measures of pulmonary function (FEV1, FVC, and PEFR). These analyses support the utility of epidural analgesia for reducing postoperative pulmonary morbidity but do not support the use of surrogate measures of pulmonary outcome as predictors or determinants of pulmonary morbidity in postoperative patients. Implications: When individual trials are unable to produce significant results, it is often because of insufficient patient numbers. It may be impossible for a single institution to study enough patients. Meta-analysis is a useful tool for combining the data from multiple trials to increase the patient numbers. These meta-analyses confirm that postoperative epidural pain control can significantly decrease the incidence of pulmonary morbidity. (Anesth Analg 1998;86:598-612)
  • Article
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    Background L-carnitine supplementation has been associated with a significant reduction in all-cause mortality, ventricular arrhythmia, and angina in the setting of acute myocardial infarction (MI). However, on account of strict homeostatic regulation of plasma L-carnitine concentrations, higher doses of L-carnitine supplementation may not provide additional therapeutic benefits. This study aims to evaluate the effects of various oral maintenance dosages of L-carnitine on all-cause mortality and cardiovascular morbidities in the setting of acute MI. Methods After a systematic review of several major electronic databases (PubMed, EMBASE, and the Cochrane Library) up to November 2013, a meta-analysis of five controlled trials (n = 3108) was conducted to determine the effects of L-carnitine on all-cause mortality and cardiovascular morbidities in the setting of acute MI. Results The interaction test yielded no significant differences between the effects of the four daily oral maintenance dosages of L-carnitine (i.e., 2 g, 3 g, 4 g, and 6 g) on all-cause mortality (risk ratio [RR] = 0.77, 95% CI [0.57-1.03], P = 0.08) with a statistically insignificant trend favoring the 3 g dose (RR = 0.48) over the lower 2 g dose (RR = 0.62), which was favored over the higher 4 g and 6 g doses (RR = 0.78, 0.78). There was no significant differences between the effects of the daily oral maintenance dosages of 2 g and 6 g on heart failure (RR = 0.53, 95% CI [0.25-1.13], P = 0.10), unstable angina (RR = 0.90, 95% CI [0.51-1.58], P = 0.71), or myocardial reinfarction (RR = 0.74, 95% CI [0.30-1.80], P = 0.50). Conclusions There appears to be no significant marginal benefit in terms of all-cause mortality, heart failure, unstable angina, or myocardial reinfarction in the setting of acute MI for oral L-carnitine maintenance doses of greater or less than 3 g per day.
  • Article
    A severely obese 28 year old woman (body mass index (BMI) 37.9) with type 2 diabetes, controlled hypertension, and sleep apnoea is seeking your advice about weight loss. She has lost 6 kg over the past year by reducing portion sizes, but her weight has recently plateaued. She does not want to consider bariatric surgery and asks instead about drug treatments. Current treatment for obesity consists primarily of health behaviour modification (diet, exercise, and behavioural therapy) for all patients and bariatric surgery for a minority of selected severely obese people.1 Because health behaviour modification is unsuccessful in many patients, and the availability of bariatric surgery is limited, additional adjunctive, effective, and safe obesity treatments are needed. To date, antiobesity drugs have not adequately filled this therapeutic void. The serotonergic agents fenfluramine and dexfenfluramine were withdrawn in 1997 because of associations with cardiac valvulopathy and pulmonary hypertension.2 After the withdrawals of rimonabant ( Acomplia ) in 2009 for depression and suicidal ideation, and sibutramine ( Meridia, Reductil ) in 2010 because of increased cardiovascular risk, orlistat became the only agent available for long term weight management. In 2012, two new oral agents—phentermine and extended release (ER) topiramate ( Qsymia ) and lorcaserin ( Belviq )—were approved by the US Food and Drug Administration as adjuvants to health behaviour modification in patients with a BMI of greater than 30 or greater than 27 if they also had an obesity related comorbidity, such as hypertension, dyslipidaemia, or type 2 diabetes. As discussed elsewhere, the European Medicines Agency did not approve either agent, citing toxicity concerns and a lack of morbidity and mortality data.3 Here, we provide a clinically focused summary to guide GPs in the use of these drugs. ### Orlistat This inhibitor of gastric and pancreatic lipase prevents intestinal fat metabolism and absorption.4 Prescription orlistat ( Xenical ) has been …
  • Article
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    We aimed to synthesize the available evidence on the relative efficacy and acceptability of specific treatments for persistent depressive disorder. We searched several databases up to January 2013 and included randomized controlled trials that compared acute pharmacological, psychotherapeutic, and combined interventions with each other or placebo. The outcome measures were the proportion of patients who responded to (efficacy) or dropped out from (acceptability) the allocated treatment. Data synthesis was performed with network meta-analysis. A network of 45 trials that tested 28 drugs included data from 5,806 and 5,348 patients concerning efficacy and acceptability, respectively. A second network of 15 trials that tested five psychotherapeutic and five combined interventions included data from 2,657 and 2,719 patients concerning efficacy and acceptability, respectively. Among sufficiently tested treatments, fluoxetine (odds ratio (OR) 2.94), paroxetine (3.79), sertraline (4.47), moclobemide (6.98), imipramine (4.53), ritanserin (2.35), amisulpride (5.63), and acetyl-l-carnitine (5.67) were significantly more effective than placebo. Pairwise comparisons showed advantages of moclobemide (2.38) and amisulpride (1.92) over fluoxetine. Sertraline (0.57) and amisulpride (0.53) showed a lower dropout rate than imipramine. Interpersonal psychotherapy with medication outperformed medication alone in chronic major depression but not in dysthymia. Evidence on cognitive behavioral analysis system of psychotherapy plus medication was partly inconclusive. Interpersonal psychotherapy was less effective than medication (0.48) and cognitive behavioral analysis system of psychotherapy (0.45). Several other treatments were tested in single studies. Several evidence-based acute pharmacological, psychotherapeutic, and combined treatments for persistent depressive disorder are available with significant differences between them.
  • Article
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    A previous meta-analysis indicated that l-carnitine significantly increased hemoglobin and decreased the required erythropoietin dose in maintenance hemodialysis patients. An updated systematic review and meta-analysis of randomized controlled trials (RCTs) was performed to reevaluate effects of l-carnitine. The Cochrane Library, PubMed, and EMBASE databases (31 December 2012) were searched to identify RCTs that investigated effects of l-carnitine in adults with end-stage kidney disease that required maintenance hemodialysis. Forty-nine RCTs (1734 participants) were included. l-Carnitine significantly decreased serum low-density lipoprotein (LDL) [mean difference (MD): -5.82 mg/dL; 95% CI: -11.61, -0.04 mg/dL] and C-reactive protein (CRP) (-3.65 mg/L; -6.19, -1.12 mg/L). There were no significant differences in triglycerides (-0.89 mg/dL; -29.32, 27.53 mg/dL), cholesterol (0.14 mg/dL; -6.15, 6.42 mg/dL), high-density lipoprotein (1.13 mg/dL; -2.44, 4.70 mg/dL), hemoglobin (0.68 g/dL; 0.14, 1.50 g/dL), hematocrit (2.04%; -1.39, 5.48%), albumin (1.65 g/L; -0.22, 3.51 g/L), or the required erythropoietin dose (-0.76 KU/wk; -1.75, 0.23 KU/wk). No adverse effects were reported. This meta-analysis failed to confirm the previous findings regarding the effects of l-carnitine on hemoglobin and the erythropoietin dose but showed that l-carnitine significantly decreased serum LDL and CRP. The extent of the decrease of LDL was not clinically relevant, whereas the significant decrease of CRP was both statistically and clinically relevant. However, the relevance of decrease of CRP with hard endpoints such as all-cause mortality and cardiovascular complications still remains to be clarified.