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Editorials

Obesity and cancer

BMJ 2007; 335 doi: https://doi.org/10.1136/bmj.39384.472072.80 (Published 29 November 2007) Cite this as: BMJ 2007;335:1107

A point of view: Hidden fat??--A matter of our serious concern !!!

A point of view: Hidden obesity?? --A matter of our serious concern!!

We read the editorial of Calle E E with interest which describes that
obesity is an important cause of type 2 diabetes mellitus, hypertension,
and dyslipidaemia. The adverse metabolic effects of excess body fat
accelerate the development of atheroma and increase the risk of coronary
heart disease, stroke, and early death. Substantial evidence supports the
link between increasing adiposity and a higher risk of many cancers.(1)

After an extensive prospective cohort study Reeves GK et al, concluded
that some colon cancers, postmenopausal breast cancers, endometrial
cancers, kidney cancers, and adenocarcinomas of the esophagus could be
prevented by avoiding weight gain.(2)

In the recent past, we critically reviewed a number of researchers' study
reports and concluded that one can have normal BMI and yet carry unseen
excess fat causing masked obesity which is not at all free from fatal
cancer risk.(3) Earlier Jennifer J. Griggs et al, also argued that the
definition of obesity itself is controversial. It is unclear whether BMI
is the most appropriate measure of obesity.BMI makes no distinction
between body weight from muscle and body weight from fat.(4)
Visceral fat is different from other body fat. It is also known as intra-abdominal fat which refers to the fatty tissues that surrounds the
internal organs or fatty degeneration within the internal organs i.e
hidden fat. Subcutaneous fat, on the other hand, is body fat accumulating
under the skin and is considered to be less dangerous, and easier to lose,
than visceral fat. Studies have shown that those with visceral fat are
more susceptible to cardiovascular dysmetabolic syndrome, type 2 diabetes
mellitus and hepatocellular carcinoma. Sedentary people, smokers and
alcoholics have been shown to have more intra-abdominal fat, or visceral
fat, than active people who are non-smokers and non-alcoholics. Stressful
life may also be a factor in the storage of visceral fat on the body.

T.Ohki et al (2009), explained that in contrast to BMI, visceral fat
accumulation is considered to be directly causative of non-B and non-C
hepatocarcinogenesis, through disturbing the adipocytokine balance of
insulin resistance, which is a major cause of hepatic fat accumulation.

Excessive fat in the liver will lead to hepatocellular injury and possibly
result in hepatocarcinogenesis through the direct cellular toxicity of
excessive free fatty acids, oxidant stress and lipid peroxidation, or some
other mechanism. Visceral fat accumulation may be involved in both tumor
initiation and promotion or progression steps through these mechanisms (5)
Impairment or inhibition of receptor molecules (PPAR-?, PPAR-? and SREBP1)
that control the enzymes responsible for the oxidation and synthesis of
fatty acids appears to contribute towards fat accumulation. In addition,
alcoholism is known to damage mitochondria and other cellular structure
further impairing cellular energy mechanism.The pathophysiological
significance of hepatic lipid accumulation in the absence of significant
alcohol consumption i.e non-alcoholic fatty liver disease (NAFLD) is now
considered the most common cause of liver enzyme elevation in Western
countries. It is regarded as the hepatic manifestation of the metabolic
syndrome (MS), characterized by central obesity and insulin resistance
(IR), and resulting diabetes type 2, dyslipidaemia and hypertension. NAFLD
encompasses mild hepatic steatosis to steatohepatitis (non-alcoholic
steatohepatitis (NASH)) with significant necro-inflammation and
progressive fibrosis. NAFLD is believed to account for a large fraction,
if not entirely for what was previously termed 'cryptogenic
cirrhosis'.Since cirrhosis is the main risk factor for hepatocellular
carcinoma (HCC), liver cancer could be simply a complication of end-stage
NAFLD. However, accumulating evidence suggests that hepatocarcinogenesis
may also be related to earlier stages of NAFLD. Considering the rapidly
increasing prevalence of both conditions in affluent societies, and their
significance in the pathophysiology of NAFLD, a rising incidence of NAFLD
and its complications--including HCC--can be expected in the mid-term
future. (6) Up to 10% of cirrhotic alcoholic FLD develop hepatocellular
carcinoma. Overall incidence of liver cancer in non-alcoholic FLD has not
yet been quantified, but the association is well established.(7)
Therefore, it is a matter of our concern that we often ignore the "spare
tire" around our waist and become victim of a number of debilitating
diseases inadvertently.

Prof (Dr) Jogenananda Pramanik MD Head of Biochemistry & Genetics and
Director of International Relations, and Tanu Pramanik BSc, MA( Sociology
) Lecturer, Pre-Medical Sciences, Allianze College of Medical Sciences,
Waziria Medical Square, Kepala Batas-13200, Palau Pinang, Malaysia.

www.acms.edu.my E-mail: jpramanik@acms.edu.my

References:

1. Eugenia E Calle,: Editorial: Obesity and cancer : BMJ 2007; 335 :
1107 doi: 10.1136/bmj.39384.472072.80

2. Reeves GK et al,: Cancer incidence and mortality in relation to body
mass index in the Million Women Study: cohort study : BMJ 2007;335:1134
doi:10.1136/bmj.39367.495995.AE

3. Jogenananda Pramanik : A mini review: Indicator of higher cancer risk--
Increased BMI or Excess hidden visceral fat depot?? ( published January
28 2011 ) www.bmj.com/letters?first-index=&hits=25&days=14&submit=Go

4. Jennifer J. Griggs, Michael S. Sabel: Obesity and Cancer Treatment:
Weighing the Evidence : Journal of Clinical Oncology, Vol 26, No 25
(September 1), 2008: pp. 4060-4062: DOI: 10.1200/JCO.2008.17.4250

5. T.ohki, R Tateisi, S Shina et al,: Visceral fat accumulation is an
independent risk factor for hepatocellular carcinoma recurrence after
curative treatment in patients with suspected NASH: Gut 2009;58:839-844
doi:10.1136/gut.2008.164053.

6. Felix Stickel, Claus Hellerbrand: Non-alcoholic fatty liver disease as
a risk factor for hepatocellular carcinoma: mechanisms and implications:
Gut 2010;59:1303-1307 doi:10.1136/gut.2009.199661

7. Qian Y, Fan JG (2005). "Obesity, fatty liver and liver cancer". Hbpd
Int 4 (2): 173-7.

Competing interests: The first author is an editorial board member of the following International Peer-Reviewed Journals: Lab-Medicine(ASCP) and Hektoen International,Chicago,USA;Social Science & Medicine,UK

01 February 2011
Jogenananda Pramanik.MD
Professor & Head of Biochemistry & Genetics
Tanu Pramanik, Lecturer
Allianze College of Medical Sciences, Waziria Medical Square,Palau Penang-13200,Malaysia.