Obesity and Headache


Women and men

Non-Asian populations

Asian populationsa
  
BMI < 18.5

BMI < 18.5

Underweight
 
BMI 18.5–24.9

BMI 18.5–22.9

Normal weight
 
BMI 25–29.9

BMI 23–24.9

Grade I obesity

Overweight

BMI 30–39.9

BMI 25–30

Grade II obesity

Severe overweight/obese

BMI ≥ 40

BMI ≥ 30

Grade III obesity

Morbid obesity


aIn 2000 the World Health Organization, the International Association for the Study of Obesity, and the International Obesity Task Force recommended that the BMI value ≥23 represents overweight status and a BMI ≥25 represents obesity in Asian populations. In 2004 the World Health Organization identified potential public health action points for a BMI between 23.0 and 27.5 in Asian populations. However, formal recommendations for BMI cutoffs for obesity status were not made, and the WHO proposed that each country make decisions regarding BMI definitions at increased risk for its population




Table 7.1b
WHO WC designations



































Men

WC < 94

Normal weight
 

WC 94–102

Action level 1

Overweight

WC > 102 cm

Action level 2

Abdominal obesity

Women

WC < 80

Normal weight
 

WC 80–88

Action level 1

Overweight

WC > 88 cm

Action level 2

Abdominal obesity


Globally approximately 13 % of adults aged 18 and older are obese (WHO Global Health Observatory (GHO) data [111]). In the United States, 35 % of women and 32 % of men have been estimated to have TBO [35]. In addition to sex, the prevalence of obesity, as well as its association with adverse health outcomes, varies by age and race. For example, while obesity is a risk factor for cardiovascular disease in younger individuals, the risk is attenuated or absent with advancing age [3, 5, 67, 103]. Further, as compared to Caucasians, Asians have greater and blacks have less body fat at the same BMI [82, 110]. Because of this, studies from China use different definitions and references for defining normal weight and obesity status which makes it challenging to compare the disease risk of obesity from different regions [23]. In 2000 the World Health Organization, the International Association for the Study of Obesity and the International Obesity Task Force recommended that the BMI value ≥23 represents overweight status and a BMI ≥25 represents obesity in Asian populations (The AsiaPacific Perspective: Redefining Obesity and Its Treatment [4, 50]). Subsequently, in 2004 the World Health Organization identified potential public health action points for a BMI between 23.0 and 27.5 in Asian populations. However, formal recommendations for BMI cutoffs for obesity status were not made, and the WHO proposed that each country make decisions regarding BMI definitions at increased risk for its population [110].

Both TBO and abd-O are comorbid with a variety of medical disorders and are associated with worse disease outcomes [1, 18]. Specifically, as has migraine, obesity has been shown to be associated with several cardiovascular and cerebrovascular risk factors, including hypertension, insulin resistance, hyperlipidemia, and pain [8, 22, 70, 84].



7.4 The Epidemiological Association Between Obesity and Headache Disorders


A body of literature supports an association between headache and obesity. In the following sections, we first discuss the existing literature examining the association between obesity and headache in general. We then separately discuss the relationship between obesity and episodic migraine, chronic migraine, and TTH.


7.4.1 General Population Studies Evaluating Obesity and Headache in General


In 2003, Scher et al. conducted the first longitudinal general population study which established a relationship between obesity and headache [92]. Scher’s study evaluated a cohort of obese and nonobese participants with episodic headaches (defined as 2–104 headaches/year, n = 1134, ages 18–65, 71 % women) as compared to those with chronic daily headaches (defined as 180 or more headaches/year, n = 798, ages 18–65, 80 % women) at baseline and again 11 months later. At baseline, obesity (sr-BMI ≥30) was 34 % more common in chronic daily headache (CDH) participants than those with episodic headache (OR 1.34, CI 1.0–1.8). Additionally, episodic headache participants with obesity were over five times more likely to transform into CDH at the 11-month follow-up visit than nonobese (sr-BMI <25) episodic headache participants (OR 5.28, CI 1.3–21.1) [92].

Subsequently, a cross-sectional analysis of 11 large general population databases (including National Health Interview Survey (NHIS), National Health Examination and Nutrition Survey, Alameda County Health Study (ACHS), Tecumseh Community Health Study (TCHS), and Women’s Health Initiative (WHI)) that included over 200,000 women 16–90+ in age demonstrated that participants with obesity (BMI 30–39.9) had an approximately 35 % increased odds of reporting headache as compared to those women with BMI = 20. Those with morbid obesity (BMI ≥ 40) were associated with an approximately 80 % increase in the odds of reporting headache [52].


7.4.2 General Population Studies Evaluating Obesity and Migraine


The first cross-sectional general population study demonstrating an association between migraine and obesity was conducted by Brown et al. utilizing the Australian Longitudinal Study on Women’s Health (ALSWH) database [17]. The ALSWH study included nearly 13,000 reproductive-aged women between 18 and 23 years and found that obese women (BMI > 30) had a 47 % (OR 1.47, 95 % CI 1.25–1.73) increased risk of having migraine or headache compared to woman of normal weight (BMI 25–29.9) [17].

Following the Brown et al. and Scher et al. studies [17, 92], Bigal et al. conducted a population-based cross-sectional analysis evaluating the relationship between obesity and episodic migraine (EM). Notably, the control group in this study included those with no headache, non-migraine headache, and possibly chronic daily headache (CDH). In this study (n = 30,215, ages 18–60+, 65 % women, obesity based on sr-BMI), those with increasing BMI were found to have increasing odds of high-frequency episodic migraine (defined as those with 10–14 headache days/month) compared to normal-weighted episodic migraineurs (BMI 30–34.9, OR 2.9, 95 % CI 1.9–4.4, BMI ≥ 35, OR 5.7, 95 % CI 3.6–8.8). However, those with obesity were not reported to be more likely to have lower frequencies of EM (i.e., ≤9 HA days/month) [10]. A second cross-sectional study by Bigal et al. in 2007 also supported an association between high-frequency EM and obesity [11].

Overall, the epidemiological literature has consistently demonstrated the importance of age and sex as modifiers of the obesity-migraine association, with data supporting the strongest association in those of predominantly reproductive age (<50–55 years; the age when migraine is most prevalent) [11, 17, 34, 79, 80, 85, 92, 108, 112, 116], [10], [78], [107] (Table 7.2), with an attenuated risk or no risk in older populations (50–55+ years) [52, 79, 80, 112, 114], [64], [113], [78] (Table 7.3). Specifically, the disease risk modification by age has been demonstrated in three separate general population cohorts (including the National Health and Nutrition Examination Survey [NHANES], the Nord-Trondelag Health Study in Norway [HUNT], and the National Comorbidity Survey Replication [NCS-R]). In the first of these studies from the NHANES (n = 21,783), men and women with migraine who were under the age of 55 showed an increase risk of migraine or severe headaches as compared to those who were nonobese (men: OR 1.38; CI 1.20–1.59; women: OR 1.39; CI 1.25–1.56). However in individuals older than 55, this risk was absent [78]. The second study to support a disease risk modification by age utilized the HUNT general population database (n = 27.945) [112]. Although age-specific cutoffs for the risk of migraine in those with obesity were not reported, the lead author (BW) was able to provide age-specific data upon request for a subsequent meta-analysis. Notably, after adjustments including age and sex, in those <50 the risk of migraine was increased by 35 % (OR 1.35, CI 1.18–1.55) in those with obesity as compared to those of normal weight; however in those 50 years or older, this risk was not present (OR 0.90, CI 0.728–1.12, data unpublished, personal communication) [112]. The third study supporting age modification of the migraine-obesity association came from the NCS-R. An almost twofold greater odds of EM in obese individuals as compared to those of normal weight (OR 1.81, CI 1.27, 2.57; p = 0.001) was demonstrated [79, 80]. This increased risk of EM in obese participants was strongest in participants who were younger than 50 years of age and women (OR 1.95, CI 1.38, 2.76; p = 0.0002) [79, 80]. Subsequently to these three studies, a meta-analysis exploring the association between migraine and BMI categories found that in obese women, the risk of having migraine was increased (PAEE 1.44, 95 % CI 1.05–1.97) as compared to normal weight women [72]. In men, considering the only two available studies, the meta-analysis was unable to find an association between migraine and obesity [72].


Table 7.2
Epidemiologic studies on migraine and obesity in predominantly reproductive-aged subjects
























































































Author (year)

Study design

(Database)

Population inclusion

Sex

Race

Mean age (range)

HA DX

BMI Dx

(SR vs M)

Findings

Brown (2000) [17]

CS-GP

(ALSWH)

Those with:

1. No HA/Mig

2. HA/Mig

n = 12,855

(HA/Mig 7229)

Women only

Not reported

88.6 % Australian

20 (18–23)

Non-ICHD

BMI: SR

The OR of HA or Mig was increased in those women who were overweight (BMI 25–29.9) or obese (BMI 30). (Overweight: OR 1.12, CI 1.00–1.25; obese: OR 1.47, CI 1.25–1.73)

Scher (2003) [92]

Long-GP

Those with:

1. 2–104 HA/year

2. CDH: 180+ HA/year

n = 1932

(EH 798, CDH 1134)

Combined sexes

White 73 %

Nonwhite 25 %

40 (18–65)

Non-ICHD

BMI: SR

1. The odds of CDH were increased in headache subjects (EH + CDH) who were overweight (BMI 25–29.9: OR 1.26; CI 1.0–1.7) or who were obese (BMI 30: OR 1.34; CI 1.0–1.8)

2. The odds of new-onset CDH was fivefold greater in those EH subjects who were obese (OR 5.28, CI 1.3–21.1) compared to normal-weighted subjects (sr-BMI 18.5–24.9)

Bigal (2006) [10]

CS-GP

(AMS)

Those with:

1. 14 or < non-migraine HA days/month

2. EM

3. CDH

n = 30,215

(EM, 3791)

Combined and stratified sex

White 72 %

Black 25 %

39 (18–89)

ICHD

BMI: SR

The odds of low frequency EM (including those groups with <3 HA days/month and those with 3–9 HA days/month) were not increased in those with obesity versus those with normal weight

The odds of high-frequency EM (i.e., 10–14 headache days/month) were increased in overweight (BMI 25–29.9: OR 1.3, CI 1.1–1.9), obese (BMI 30–35: OR 2.9, CI 1.9–4.4), and morbidly obese groups (BMI ≥35: OR 5.7, CI 3.6–8.8) compared to those with normal weight (BMI 18.5–24.9)

Bigal (2007) [11]

CS-GP

(AMPP)

Those with:

1. EM and probable Mig

2. SETTH

3. Other EH

4. No HA (unknown if CDH was included or excluded)

n = 162,576

(EM, 18,968)

Combined and stratified sex

White 87.5 %

Black 6.2 %

Others 3.4 %

Unknown 3.0 %

40–49 (12–70+)

ICHD2

BMI: SR

The odds of high-frequency EM (i.e.,10–14 headache days/month) were increased in overweight (BMI 25–29.9: OR 1.15, CI 0.98, 1.13), obese (BMI 30: OR 1.3, CI 1.1, 1.5), and morbidly obese groups (OR 1.7, CI 1.4, 1.9) as compared to EM participants of normal weight (BMI 18.5–24.9)

Ford (2008) [34]

CS-GP

(NHANES)

Those with:

1. Severe HA or Mig

2. No severe HA or Mig

n = 7601

(EM, 1649)

Combined and stratified sex

White 50 %

Black 18 %

Mex-Am 24 %

46 (20–85)

Non-ICHD

BMI: M

The odds of migraine or severe headaches were increased in those with obesity (BMI ≥ 30) as compared to normal-weighted (BMI 18.5–25) episodic migraineurs (OR 1.37, CI 1.09, 172)

Peterlin (2010) [78]

CS-GP

(NHANES)

Those with:

1. Severe HA or Mig

2. No severe HA or Mig

n = 15,631(≤55 years)

(EM, 3915)

Stratified

White 70–82 %

Black 8–11 %

38 (20–55)

Non-ICHD

BMI: M

1. The odds of migraine or severe headaches were increased in obese women (BMI 30, OR 1.39, CI 1.25, 1.56) and obese men (BMI 30, OR 1.38, CI 1.20, 1.59) as compared to nonobese (BMI < 30) women and men

2. The odds of migraine or severe headaches were increased in abd-O women (OR 1.26, CI 1.1–1/45) and abd-O men (OR 1.3, CI 1.13–1.49) as compared to women and men without abd-O

Robberstad (2010) [85]

CS-GP

(HEAD-HUNT YOUTH)

Those with:

1. Mig

2. TTH

3. Non-classifiable HA

4. No HA in past 12 months

n = 5847

(EM, 392)

Combined and stratified

White 98 %

Nonwhite <3 %

≤18 (13–18)

Non-ICHD

BMI: M

The odds of migraine were increased in adolescent and young adults who were overweight or obese (OR 1.6, CI 1.4, 2.2) as compared to those of normal weight

Note: obesity status was defined based on pediatric cutoff points

Vo (2011) [107]

CS-GP

(OMEGA)

Those who:

1. Received a Mig Dx

2. Never Dx with Mig

n = 3733

(EM, 672)

Women

White 86 %

Others 14 %

<40 (18–40s)

Non-ICHD

BMI: SR

The odds of migraine were increased in obese (BMI ≥ 30) premenopausal women as compared to those of normal weight (BMI 18.5–24.9) and which increased with increasing obesity status (BMI 30–34.9: OR = 1.48; CI 1.12, 1.96; BMI 35–39.9: OR 2.07; CI 1.27, 3.39; BMI ≥40: OR 2.75; CI1.60, 4.70)

Winsvolda (2011) [112]

CS-GP

(HUNT)

Those with:

1. Mig

2. No Mig

n = 16,319

(Mig, 2728)

Combined

Not reported

20– < 50

ICHD

BMI: SR

The odds of migraine were increased in obese (BMI ≥ 30) participants as compared to those of normal weight (BMI 18.5–24.9: OR 1.29, CI 1.14, 1.46) and remained significant after adjustment for age, sex, and education (OR 1.35, CI 1.18, 1.55)

Yu (2012) [116]

CS-GP

Those with:

1. EM (<15 HA days/month)

2. No EM (excluded those with headache ≥15 days/month)

n = 5029

(EM, 467)

Combined

Han Chinese 94 %

Others 6 %

43 (18–65)

ICHD2

BMI: M

The odds of EM were increased in Asians with morbid obesity (BMI ≥ 30; OR 2.10, CI 1.39–3.12) as compared to Asian individuals of normal weight (BMI 18.5–23)

Note: in Asian populations normal weight is estimated as a BMI of 18.5–23, obesity a BMI ≥25, and morbid obesity a BMI ≥30. See Tables 7.1a and 7.1b for complete BMI categories for obesity status in Asian populations

Peterlin (2013) [79]

CS-GP

(NCS-R)

Those with:

1. Active EM (≤168 HA days/year)

2. Never had HA or Mig

n = 2265

(EM, 149)

Combined and stratified

White 85.5 %

Black 14.5 %

<50 (18–50)

ICHD2

BMI: SR

The odds of EM were increased in those who were obese (OR 1.86, CI 1.20, 2.89) as compared to individuals of normal weight (BMI 18.5–24.9)

The odds of EM increased with increasing obesity status from normal weight to overweight to obese (p = 0.001)

Wang (2015) [108]

CS-GP

Those with:

1. Migraine (<15 HA days/month)

2. TTH

3. CDH (≥15 HA days/month)

4. No headache

n = 1023

(EM, 152)

Women only

Han Chinese 95.3 %

Non-Han 4.7 %

20–29 (20- > 40)

ICHD3-beta

BMI: SR

The unadjusted odds of EM were increased in those who were obese (BMI ≥ 25) as compared to individuals of normal weight (BMI 18.5–22.9), OR 1.86, CI 1.04, 3.34, p < 0.05. However, this was no longer significant after adjustments including age, seniority, and nursing specialty

Note: in Asian populations normal weight is estimated as a BMI of 18.5–23, obesity a BMI ≥25, and morbid obesity a BMI ≥30. See Tables 7.1a and 7.1b for complete BMI categories for obesity status in Asian populations


AbdO abdominal obesity (defined as WC ≥102 cm in men; WC ≥88 cm in women), CI confidence interval, CS cross-sectional. Long longitudinal, EH episodic headache, EM episodic migraine, GP general population study, HA headache, MexAm Mexican American, OR odds ratio, M measured, SR self-reported, Mig migraine, SETTH severe episodic tension-type headache

aData unpublished, personal communication



Table 7.3
Epidemiologic studies on migraine and obesity in predominantly peri-postmenopausal-aged subjects


























































Author (year)

Study design

(Database)

Population

Inclusion

Sex

Race

Mean age

(range)

HA

BMI Dx

(SR vs M)

Findings

Mattsson (2007) [64]

CS-GP

(Swedish database)

Total: 684

EM: 130

Women only

Not reported

54

(40–74 years)

IHS

BMI:

M

Obesity was not associated with migraine in older women

Keith (2008) [52]

CS-GP

(WHI) a

Total: >220,370

EM: not reported

Women only

White 83 %

>50

(50–79 years)

Non-ICHD

BMI:

M

Obesity was not associated with migraine in older women

Winter (2009) [113]

CS-GP

(WHS)

Total: 63,467

EM: 9195

Women only

Not reported

54

(≥45 years)

Non-ICHD

BMI:

SR

Obesity was not associated with active migraine or prior history of migraine in older women

Peterlin (2010) [78]

CS-GP

(NHANES)

Total: 6152

(>55 years)

EM: 749

Both

Men: white 81.8 %

Black 8.2 %

Women: white 79.8 %

Black 9.1 %

68

(≥55 years)

Non-ICHD

BMI:

M

Obesity was not associated with migraine in older women or men

Winsvoldb (2011) [112]

CS-GP

(HUNT)

Total: 15,031

Mig: 677

Both

Not reported

≥50

ICHD

BMI:

SR

Obesity was not associated with migraine in older women or men

Winter (2012) [114]

Long-GP

(WHS)

Total: 19,162

EM: 3483

Women only

White 95 %

54

(≥45 years)

Non-ICHD

BMI:

SR

Neither obesity nor weight gain was associated with migraine in older women

Peterlin (2013) [79, 80]

CS-GP

(NCS-R)

Total: 1356 (aged > 50)

EM: 39

M 49.7 %

F 50.3 %

White 85.5 %

Black 14.5 %

>50

(50–98 years)

ICHD2

BMI:

SR

Obesity was not associated with episodic migraine in older women or men


CS cross-sectional, EM episodic migraine, Long longitudinal, GP general population, mBMI measured BMI, srBMI self-reported BMI

aThis study was a meta-analysis evaluating the association between headache in general and obesity; however only the WHI database was used when evaluating the association between obesity and migraine specifically

bData unpublished, personal communication

In addition to age and sex, race likely has a relevant role in the association between migraine and obesity as well. Two studies investigated the possible association between migraine and obesity in Asian subjects, both of which used a BMI ≥ 25 as the cutoff for obesity. (Note: Obesity in Asian populations is accepted as BMI ≥25, whereas morbid obesity is classified as BMI ≥30; see Table 7.1a.) The first of those two studies included more than 5000 participants aged 18–65 years in China. Although not in Chinese individuals with grade I obesity (BMI 25–29.9), those with morbid obesity (BMI ≥ 30) had a twofold increase in the risk of migraine (OR 2.1, 95 CI 1.4–3.2) as compared to those classified as normal weight participants (BMI 18.5–23.0 kg/m2) [116]. A second study in China, involving around 1100 female nurses ages > 20, found that those with obesity (BMI ≥ 25) had an 86 % increased risk of migraine (OR 1.86, 95 % CI 1.04–3.34, p < 0.05) compared to those of normal weight (BMI 18.5–22.9). However, this did not remain significant after adjustments for age, seniority, and nursing specialty (OR 1.5, 95 % CI 0.8–2.8) [108].

Only one general population study has attempted to look at the disease modification of the migraine and obesity association in whites versus blacks. In the general population study utilizing the National Comorbidity Survey Replication, while the odds of EM were increased by 81 % (OR 1.81, 95 % CI 1.27–2.57; p < 0.001) in those with obesity when including both black and white participants, the odds of EM were twofold higher when analyses were limited to only white participants (OR 2.06, CI 1.41–3.010) [79, 80].


7.4.3 General Population Studies Evaluating Obesity and Chronic Migraine


In addition to episodic migraine, there is also an association between chronic migraine and obesity. After Scher et al. demonstrated an increased risk for obese individuals to develop chronic headache [92], Bigal and Lipton further confirmed this relationship with a large population-based cross-sectional study of more than 30,000 participants (ages 18–89, female 62 %, headache diagnosis based on ICHD, obesity based on sr-BMI) [10]. As in the Scher study, investigators noted a significant association between increasing categories of sr-BMI and increasing odds of chronic migraine [10]. Specifically, there was a 1.5-fold increased odds for having chronic migraine in those with BMI between 30 and 34.9 (OR 1.5, CI 1.2–1.8) and a twofold increased odds for having chronic migraine in those with BMI > 35 (OR 2.0, CI 1.4–2.4) compared to those of normal weight (BMI 18.5–24.9) [10]. In addition, a recent large general population cross-sectional study based on the German Headache Consortium cohort (n = 6992, ages 18–65, 50 % women, headache diagnosis based on ICHD2, obesity based on sr-BMI) showed that chronic migraine participants were more likely to be obese (sr-BMI >30) compared to those without headache (OR 1.72, 95 % CI 1.02–2.92) [93]. However, this did not remain significant after adjustments for pain medication use (OR 1.85, 95 % CI 0.54–6.27) [93]. In the most recent study including more than 15,000 participants aged 35–74 years, investigators showed an increased risk of daily migraine in obese as compared to normal weight participants (OR 1.9, 95 % CI 1.1–3.1) [89]. The pooled analysis of the two comparable studies [10, 89] indicated that overweight was associated with 40 % increase in the risk of chronic migraine (PAEE 1.4, 95 % CI 1.1–1.7), and obesity was associated with 80 % increase in the risk of chronic migraine (PAEE 1.8, 95 % CI 1.3–2.3) [72].


7.4.4 General Population Studies Evaluating Obesity and Tension-Type Headache (TTH)


The association of obesity with TTH is not as clear as that between obesity and migraine, with some data suggesting a connection [108, 112], while other studies unable to prove the association [11, 93, 114]. Winsvold et al. in a cohort of nearly 50,000 subjects aged ≥20 years found a 20 % increased risk of non-migrainous headache among obese participants as compared to normal weight participants (OR 1.2, 95 % CI 1.1–1.3) [112], though it did not specify TTH by ICHD diagnosis. However, in [11] study, while CTTH has been found to be more prevalent in those morbidly obese compared to those normal weight (4.3 %, OR 1.4, CI 1.1–1.9), episodic tension-type headache has not been found to be significantly associated with obesity (sr-BMI) [11]. Finally, Robberstad et al. reported a 40 % increased risk of TTH (episodic and chronic together) in adolescents 13–18 years of age who were overweight or obese (OR 1.4, 95 % CI 1.1–1.6) [85].


7.5 Central and Peripheral Associations Between Migraine and Obesity


As discussed above, obesity has been reported to be a risk factor for headache in general, as well as in both episodic migraine and chronic migraine. The obesity-migraine association is greater in women as compared to men and younger as compared to older individuals [22]. There is only a weak association between tension-type headache and obesity. The current epidemiological literature on this association does not allow us to identify the direction of the association, as only two separate databases have been utilized to examine this association longitudinally, one which did not include non-headache controls [92] and the second only examined older women (age ≥45, from the WHS) [114].

While the directionality of the migraine-obesity association has not yet been clarified, factors such as medication side effects and exercise likely contribute to or modify this relationship. Weight gain is a common side effect of many frequently used migraine prophylactic medications [96]. It is conceivable that medication-related weight gain is at least in part contributing to the prevalence of obesity among migraineurs. Additionally, lack of physical activity has been linked with increased migraine attacks. More specifically, lack of exercise has been demonstrated to be associated with a 21 % increased risk of headache attacks in adult migraineurs (HR 1.209; p < .01) [115] and a 50 % increased risk of migraine in adolescents (OR 1.5, 95 % CI 1.0–2.2) [85]. Additionally, obese migraineurs were found to spend less time engaging in physical activity than obese participants without migraine [14]. Therefore a more sedentary lifestyle may be a common link between obesity and worsening headache in migraineurs.

Alternatively, or in addition, there are several plausible shared mechanisms between the regulations of feeding/adiposity and that of pain/migraine pathogenesis, which may also help to explain the obesity-migraine association. Adipose tissue is an active endocrine organ with roles in energy homeostasis, reproduction, as well as inflammation [99]. In the following section, we review the central and peripheral pathways regulating feeding and adipose tissue function and discuss the extensive overlap of pathways implicated in both obesity and migraine.


7.5.1 Central Regulation of Feeding and Its Overlap with Migraine Pathophysiology


The regulation of feeding is controlled by the “melanocortin system.” The melanocortin system is composed of the arcuate nucleus (ARC) of the hypothalamus and its connections [16]. The ARC contains orexigenic and anorexigenic neuropeptides [25, 26]. Signals from the ARC neurons are transmitted to several other hypothalamic nuclei, including the paraventricular nucleus (PVN), which express adiponectin and leptin receptors, as well as to the ventromedial (VM) and lateral hypothalamus (LH) nuclei [16, 25, 26, 99]. In the LH, there are two groups of neurons, the orexin neurons, which stimulate feeding, and the melanin-concentrating hormone (MCH) neurons, which inhibit food intake. These neurons subsequently project to the brainstem nuclei, the nucleus tractus solitarius (NTS), and the dorsomotor nucleus of the vagus (DMV), where the descending hypothalamic inputs are integrated with the peripheral inputs from the liver and gastrointestinal tract [16, 25, 26].

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Oct 25, 2017 | Posted by in NEUROLOGY | Comments Off on Obesity and Headache

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