





































Clinical Medicine Insights
Received 25 Dec 2020 | Revised 22 Jan 2021 | Accepted 28 Feb 2021 | Published Online 30 Mar 2021

DOI: https://doi.org/10.52845/CMI/2021-2-1-4 
CMI JOURNAL 2 (1), 80−97 (2021) ISSN (O) 2694-4626 

REVIEW ARTICLE

Obesity and Non-Communicable Diseases: Part II Cancer, Diabetes 
Mellitus, Kidney Diseases, Alzheimer’s Disease, Arthritis

Shashi K. Agarwal, MD ∗
 

12227 US Highway 1, #309 North
Brunswick, NJ 08902,USA

Abstract
Obesity is increasing all over the world. An excess body weight,
as recognized by a body mass index of more than 25, is associated
with several chronic diseases, increased disability, and early mortality.
Its main impact is on non-communicable diseases, such as cancer,
diabetes mellitus, kidney diseases, Alzheimer’s disease, and arthritis.
Successful weight loss strategies through healthy lifestyle behaviors
and bariatric surgery have been associated with a decrease in morbidity,
an improved quality of life, an increase in disease-free years, and
improved longevity.
Keywords: obesity, non-communicable diseases, cancer, diabetes mel-
litus, chronic kidney disease, dementia, arthritis

Copyright : © 2021 The Authors. Published by Medical Editor and
Educational Research Publishers Ltd. This is an open access article
under the CC BY-NC-ND license
(https://creativecommons.org/licenses/by-nc-nd/4.0/).

1 INTRODUCTION

The prevalence of overweight and obesity is
increasing globally and is expected to reach
1.35 billion and 573 million respectively by

20301. Major health organizations recommend that
a healthy lifestyle should include adherence to a
normal body weight (a body mass index or BMI
of 18.5–24.9 kg/m2), regular physical activity (150
min/week of moderate to vigorous physical activity),
and a healthy diet (ideally 32 g/day of dietary fiber,
400 g/day of fruit and non-starchy vegetables, 0
g/week of processed meat, and <500 g/week of red
meat), and avoidance of smoking and moderation

in alcohol intake2. Healthy lifestyles help not only
prevent but also help decrease the undesirable impact
of several diseases3−5. Besides a reduction in mor-
bidity, the overall health quality of life is improved
in these patients and mortality is decreased6−8. Li
et al. using data from the Nurses’ Health Study and
the Health Professionals Follow-up Study (total of
123,219 participants), estimated that adherence to all
five healthy lifestyles increases the lifespan at age 50
by 14 years in females and 12.2 years in males, when
compared with those with zero low-risk factors9. A
normal body weight is a major lifestyle factor in
the prevention of noncommunicable diseases10. As
mentioned in Part I of this manuscript, a BMI be-

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SHASHI K. AGARWAL, MD

tween 25 and 29.9 kg/m2 is considered overweight,
while a BMI of >30 kg/m2 is considered obese11. The
Global Burden of Disease project, in a metanalysis of
239 prospective studies in four continents, reported
a J shaped relationship between BMI and all-cause
mortality12. This research included >10 million peo-
ple and recorded 385,879 deaths during amedian fol-
low up of 13.7 years12. The lowest mortality was in
individuals with a BMI of 20.0 to 25.0 kg/m212. All-
cause mortality increased both below and above this
BMI range12. The most dramatic increase in mor-
bidity and mortality was noted in individuals who
became obese12. Obesity is further divided into class
1 (30.0-34.9 kg/m2), class 2 (35.0-39.9 kg/m2), and
class 3 (40 kg/m2 or greater)13. Mortality increases as
the class of obesity increases12. The Global Burden
of Disease project reported that mortality increased
by 45% for grade I obesity, by 94% for grade 2
obesity, and 176% for grade-3 obesity12. The ben-
eficial effect of weight loss has also been reported14.
The Swedish Obese Subjects Study showed a 29%
reduction in overall mortality (after 10.9 years of
monitoring) in obese patients who underwent surgi-
cal intervention for obesity14.
The problems associated with obesity in several
chronic medical conditions are discussed in this two-
part manuscript. Part I discussed the role of obesity in
cardiovascular diseases (CVD), chronic respiratory
diseases, depression, and liver diseases. This part dis-
cusses its effect on cancer, diabetes mellitus, kidney
diseases, Alzheimer’s disease, and arthritis.

2 DISCUSSION

Noncommunicable diseases (NCD) are common
conditions affecting humans15. Cancer has become

Supplementary information The online version 
of this article (10.52845/CMI/2021-2-1-4) contains 
supplementary material, which is available to autho-
rized users.

Corresponding Author: Shashi K. Agarwal, MD 
Shashi K. Agarwal, MD 2227 US Highway 1, #309 
North Brunswick, NJ 08902,USA
Email: usacardiologist@gmail.com

the king of all maladies and is on its way to replacing
CVDs as the number one killer in the world16. It is es-
timated that 1 in 5 men and 1 in 6 women developed
cancer in 2016, resulting in the deaths of 1 in 8 men
and 1 in 10 women17. The most common global can-
cers are those involving the lung, colorectum, stom-
ach, breast, prostate and liver17. Type 2 Diabetes
Mellitus (DM) is one of the most common metabolic
disorders worldwide18. It results from a combina-
tion of reduced insulin secretion by pancreatic β-
cells and peripheral insulin resistance19. Prediabetes
is associated with an increased risk of developing
DM20. This disease is associated with significant
microvascular (retinopathy, nephropathy, and neu-
ropathy) andmacrovascular (coronary artery disease,
stroke, peripheral artery disease) pathology21. It re-
duces the life expectancy of the affected individual
by approximately six years22. Cardiovascular disease
is extremely common in diabetics and cardiovascular
complications are responsible for more than 50% of
diabetes related deaths23. Diabetes is now considered
an independent risk factor for CVD24. Prediabetes is
also associated with a higher risk of atherosclerotic
cardiovascular disease and all-cause mortality25.
Chronic kidney disease (CKD) is defined by the pres-
ence of kidney damage or an estimated glomerular
filtration rate (eGFR) less than 60 ml/min/1.73 mt2,
persisting for 3 months or more, irrespective of the
cause26. It has become a worldwide public health
problem27. DM is the leading cause28. CKD is a
progressive disease, and as it worsens, the affected
individuals need peritoneal dialysis or hemodialysis
or kidney transplantation29. It affects most systems
of the body and often leads to atherosclerotic car-
diac disease, poor cognitive dysfunction, and a poor
quality of life30−32. Dementia is a common world-
wide disease33. Alzheimer’s disease (AD) is themost
common form of dementia and is responsible for
about 70% of the cases34. AD is a progressive
and irreversible neurodegenerative disease, asso-
ciated with amyloid plaques and neurofibrillary
tangles in the brain35. The World Alzheimer Re-
port estimates that 50 million people worldwide
have dementia, and this number is projected to
increase to 82 million by 2030 and to 152 million
by 205036. It leads to loss of independence, poor
quality of life, and premature institutionalization37.

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OBESITY AND NON-COMMUNICABLE DISEASES: PART II CARDIOVASCULAR DISEASES, 
RESPIRATORY DISEASES, DEPRESSION, LIVER DISEASES
It is also a major cause of death38. Treatment re-
mains symptomatic, as a definitive cure is lacking39.
Arthritis is of many types40. Osteoarthritis (OA) is
the most common type and a major global cause
of disability41. It is characterized by progressive car-
tilage degradation, synovitis, osteophyte formation,
and subchondral bone sclerosis42. It usually affects
the knees and the hip and is associated with consid-
erable pain and disability43,44. Rheumatoid arthritis
(RA) is an autoimmune arthritis and is character-
ized by symmetrical polyarthritis oftenwith systemic
manifestations45. Gout is an autoinflammatory joint
arthritis, induced by monosodium urate crystals that
are deposited in joints (and soft tissues)46. Hype-
ruricemia is usually the underlying abnormality47.
Gout and hyperuricemia are both rising globally48,49.

2.1 CANCER

Obesity has been linked to an increased risk for
several cancers, including those of the breast (post-
menopausal), colon and rectum, corpus uteri (en-
dometrium), esophagus (adenocarcinoma), gallblad-
der, kidney, liver, meningioma, multiple myeloma,
ovary, pancreas, stomach (cardia), and thyroid50. A
recent report from the World Cancer Research Fund
and the American Institute for Cancer Research also
indicated a potential link between body fatness and
advanced prostate cancer and cancers of the mouth,
pharynx, and larynx51. Excess body weight and can-
cer is more than twice as high in women (368,500
cases) as in men (175,800 cases)52. Males demon-
strate an increased risk for neoplasms of the colon,
rectum, and prostate, while women have an increased
risk for cancers of the breast, endometrium, and
gallbladder53. Islami et al estimated that excess body
weight was associated with 60.3% of uterine cancers,
33.9% of liver cancers, 11.3% of breast cancers in
women, and 5.2% of colorectal cancers54. Lauby-
Secretan et al. estimated that an increase of every
5 kg/m2 rise in body mass index resulted in a 5%
increase in the risk of colorectal cancer and a 50%
increase in the risk of endometrial cancer55. Central
obesity is also positively associated with cancer56.
Obesity induces a more rapid cancer progression57,58
and is associated with reduced efficacy of certain
drugs59. Obese patients also have more cancer recur-

rences and tend to develop secondary primary can-
cers more often60. Obesity cancer survivors report
a reduced quality of life61,62. Obesity is also associ-
ated with decreased survival, both in children63 and
adults64. Morbidly obese patients (BMI >40) exhibit
a 52% higher mortality rate in men and a 62% higher
mortality rate in women, when compared to those
with normal weight65.
Obesity contributes to a pro-carcinogenic environ-
ment by producing a pro-inflammatory state66, ini-
tiating several sex and growth hormonal changes67,
increasing blood levels of insulin and insulin-
like growth factor-168, promoting oxidative stress69,
cell proliferation and angiogenesis70, and inhibiting
apoptosis/cell death71. Mechanical effects of excess
fat may also play a role in some cancers72.

2.2 DIABETES MELLITUS

Studies indicate that more than 85% of people with
DM are overweight or obese73. This number is on
the increase, and it is estimated that by 2025, more
than 300 million people worldwide will have DM
associated with obesity74. Scientific data reveals that
an increase in BMI, central obesity and an increase
in body weight prognosticate the development of
DM75−77. A study from the UK found that the risk
of developing future DM was four times higher
in obese children and obese adolescents78. Weight
loss helps79. In the Diabetes Prevention Program, a
median weight loss of 5.5% over 2.8 years reduced
the risk of converting from prediabetes to diabetes
by 58%80. Bariatric surgery not only results in a
weight loss of 20% to 30% but also induces DM
remission rates ranging from 23% to 60%81. In the
Look AHEAD (Action for Health in Diabetics) trial,
besides a lower AIC and a reduced need for diabetic
medications, patients also reduced their hospitaliza-
tions and health care costs, besides experiencing a
reduction in sleep apnea, improved mobility, and a
better quality of life82,83. Weight reduction is asso-
ciated with an improvement in cardiovascular mor-
bidity and mortality in these patients84. In a more
recent DIRECT trial, weight loss was associated with
sustained remissions of DM in more than a third
of people at 24 months85. Obesity causes chronic
inflammation, biotoxicity and adipocyte induced loss

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of insulin sensitivity, and these factors contribute to
the development of DM86.

2.3 KIDNEY DISEASES

Obesity is a major cause of chronic kidney disease
CKD87−94. A high BMI is often associated with
the presence of proteinuria in individuals without
kidney disease95−98. Furthermore, in numerous large
population-based studies, high BMI appears to be
associated with the development of low eGFR99,100.
Obesity is also associated with a more rapid pro-
gression of the disease. often leading to end stage
renal disease (ESRD)101−109. Obese patients have
a higher risk of complications during and after renal
transplantation surgery110. As noted with CVDs and
DM, central obesity seems to be more important
than BMI as a risk factor for CKD in several cross-
sectional studies111. A waist circumference (WC)
>102 cm and a waist hip ratio (WHR) of 0.9 in
females, and a WC >88 cm and WHR >0.8 in males,
is associated with an increased risk of CKD, even if
the BMI is normal112. Higher abdominal girth has
been associated with albuminuria113,114, decreased
eGFR115, and a higher incidence of ESRD116, in-
dependent of BMI level. Visceral obesity (BMI-
independent) also predicts poorer renal outcomes,
including mortality in patients with ESRD117 and
after kidney transplant118.
Weight loss helps kidney disease119−125. In obesity
related glomerulopathy, a weight loss of 12% re-
sulted in a decrease in proteinuria by >80%119.
Weight loss with bariatric surgery also results in
improvement in kidney function120−125. An asso-
ciation between obesity and nephrolithiasis has
also been described, particularly with uric acid
and calcium oxalate calculi126−129. Obesity is also
associated with an increased risk of cancer of the
kidney130,131. In a meta-analysis, Guh et al estimated
that this increased risk was 1.82 for men and 2.64 for
women132. Despite the deleterious effects of obesity
on CKD and its progression, several studies have
noted that obesity may result in lower mortality rates
in patients with advanced CKD and ESRD133−136.
This obesity paradox in these individuals may reduce
mortality by providing better protein and energy
reserves, a higher muscle mass with enhanced an-

tioxidant capacity, and lower circulating actin and
higher plasma gelsolin levels137,138.
Obesity impacts the kidneys via production of
adiponectin, leptin and resistin139−141. There are
more inflammatory cytokines141, increased oxida-
tive stress142, abnormal lipid metabolism143, activa-
tion of the renin-angiotensin-aldosterone system144,
and increased production of insulin with insulin
resistance145,146. There may be a direct pressure
effect of the increased perirenal fat also.147 Obe-
sity is also closely associated with DMs, HTN, and
atherosclerosis, which are also important risk factors
for CKD148,149.

2.4 ALZHEIMER'S DISEASE

The relationship between increased BMI and de-
mentia is well established150,151. In a review of 19
longitudinal studies including 589,649 people aged
35 to 65 years, followed up for up to 42 years,
obesity was associated with late life dementia150.
This was also reported in another metanalysis (1.3
million adults aged ≥18 years) where a higher body
mass increased the dementia risk by a RR of 1.3151.
A systematic review and a meta-analysis also re-
ported a link between obesity and AD152,153. Xu et
al. reported that obese individuals at midlife de-
veloped dementia at a mean odds ratio of 3.88154.
Visceral obesity is also pathogenic for AD155,156.
In a longitudinal study of 6,583 individuals, those
with the largest abdominal diameter appeared
to have a three-fold risk of developing demen-
tia, when compared with those with the small-
est diameter155. Another study observed that a
larger waist-hip ratio was associated with de-
creased hippocampal volume156, the latter often
seen in patients with AD157. Although some stud-
ies have noted that older people often have low
body weight when they exhibit dementia, this
low body weight is often deceptive as a causative
factor158,159. It seems that dementia often takes 10
years to set in and during this time, BMI may de-
cline in these individuals due to comorbidities and
otherwise poor health160. Although other lifestyle
changes help, weight loss also plays an important
preventive and therapeutic role in AD161. It has
been projected by an Australian study that in

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2050, dementia in old age can be reduced by 10%
by decreasing midlife obesity by 20%162. A meta-
analysis of seven RCTs (468 participants) and 13
longitudinal studies (551 participants) of overweight
and obese adults without dementia, (mean age 50
years), reported that weight loss of 2 kg or more
in people with BMI greater than 25 was associ-
ated with a significant improvement in attention and
memory163.
Obesity is also a well-known risk factor for
DM164, dyslipidemia165, cardiovascular diseases166,
and cerebrovascular diseases167 - all known risk
factors for AD. Obesity induces adipokine dys-
regulation leading to central nervous system
inflammation168−172. The resultant increase in
microglia causes reduced synaptic plasticity and
impaired neurogenesis173. Microglia also interfere
with insulin action and can result in Aβ accumulation
and reduce the tau protein degradation seen in AD173.

2.5 ARTHRITIS

Obesity is commonly seen in patients with knee
and hip osteoarthritis174.Obesity is traumatic to
the knees175. The excessive joint loading in obese
patients is thought to alter gait and movement
strategies, resulting in joint malalignment and
cartilage degeneration176. Obese patients under-
going total knee arthroplasty experience increased
revision rates, lower functional scores, and in-
creased complications, including infection, when
compared to non-obese patients177−179. Obese indi-
viduals also suffer from increased osteo-arthritis
of non-weight bearing joints180. The actions of
pro-inflammatory adipokines and cytokines are
implicated in this181. Obesity is also significantly
associated with RA182−184.A meta-analysis of 11
studies concluded that obese patients had a rel-
ative risk of 1.31 for RA185. Females are at a
higher risk when compared to males186,187. Cen-
tral obesity, even with normal BMI, appears to
be worse in this relationship188. Obesity also dele-
teriously impacts RA progression throughout the
course of the disease189,190. In a meta-analysis, Liu
et al found that obese patients had decreased
remission during therapy and overall experienced
poorer outcomes191. Interventions to prevent and re-

verse obesity help improve the outcomes and quality
of life in RA patients191. Obese patients with RA
also exhibit higher comorbidity rates, negatively
affecting RA prognosis192. The major damage
is conveyed by adiposity related adipocytokines,
which exert pro-inflammatory effects193,194. Sev-
eral other potential mechanisms, such as vitamin
D deficiency, sex hormone differences, and in-
sulin resistance, may also play a role195. Gouty
arthritis is also causally connectedwith obesity196.
In an evaluation of 10 prospective studies, in-
volving 27,944 cases with a median follow-up of
10.5 years, Aune et al. found that the relative
risks for gouty arthritis were 2.67, 3.62, and 4.64
for people with a BMI of 30, 35, and 40 kg/m2,
respectively, compared with people with a BMI
of 20 kg/m2196.

3 CONCLUSION

Obesity has a causal relationship with most major
NCDs197. Obese children usually end up being obese
in their adult life198. The increasing prevalence of
obesity in children and adolescents portends an in-
crease an increase in NCDs during adulthood in these
individuals199. The evidence for the preventive and
therapeutic effects of maintaining a normal BMI is
persuasive200. Most studies also reveal the benefits
of weight loss on NCDs, including via bariatric
surgery79,120,162. It is therefore clear that obesity is
an important lifestyle that needs to be targeted to
decrease the NCD burden, both in children, adoles-
cents, and adults.
Acknowledgment: None
Funding: None
Conflict of interest: None
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How to cite this article: Agarwal S.K,, MD. 
OBESITY AND NON-COMMUNICABLE 
DISEASES: PART II Cancer, Diabetes 
Mellitus, Kidney Dis-eases, Alzheimer’s Disease, 
Arthritis. Clinical Medicine Insights. 2021;80
−97. https://doi.org/ 10.52845/CMI/2021-2-1-4

MEERP LTD CMI JOURNAL 2 (1), 80−97 (2021) 97


	Introduction
	Discussion
	CANCER 
	DIABETES MELLITUS 
	KIDNEY DISEASES
	ALZHEIMER'S DISEASE
	ARTHRITIS

	CONCLUSION



