4 Conclusions and Recommendations
4.3 Recommendations
The im portance of the knowl edge of Bod y Mass Index in rel ati on to the control of s om e dis ease conditi ons has been demonst rated by s om e studies.
Stroke has been found to be lowes t at Bod y M as s Index 20 – 21.9. Combined risk of death from an y cause, heart att ack, stroke and di abetes was l east at Bod y Mass Index (BM I) 20 – 24 2 6 , 2 7.
H ypertension is one of t he known cardi ovas cul ar probl ems of obesit y.
Obesit y cause s increas e in cardi ac out put, heart rate, st roke volum e, blood volum e and cardiac work. In addition, the h yperl ipidaemi a t hat occurs i n obesit y can lead to atherom a (deposition of fatt y plaques i n the i ntim a of blood vess els ). Thes e are known ris k fact ors for h ypert ensi on 2 , 2 8 , 2 9. It coul d also be t hat the presence of all thes e factors i nduce s uffi ci ent st ress i n the indivi dual t o produce a s ust ained el evat i on of blood press ure.
Another pos sibl e m echanism t hat has been suggest ed i s that wei ght gai n and blood press ure el e vati on m a y be the int erm ediat e phenot ypes of an underl yi ng s ym pathetic overactivit y in h ypert ensi on. The expl anation for this is that stimulation of β – adrenergic receptors increases total body energy expenditure. A chronic i ncreas e in s ym pat heti c tone ca us es downregul ation of β – adrenergic receptors. A decreased cardiac, vascular, glucose and phosphate response to β – agonist has been described in hypertension. If this decreased β – adrenergic responsiveness were generalized to energy expenditure, h ypert ensives will have a di minished abilit y to dissipat e ex cess calories, t his would resul t in wei ght gai n2 9 , 3 0 , 3 1.
35
Moreover, whil e overwei ght and wei ght gains are associ ated wi th h ypert ension, in some subj ects, h ypert ensi on has preceded wei ght gai n. It was th erefore s uggested that t his m a y be the reason wh y i n spit e of honest efforts and motivati on from ph ys i ci ans , h ypert ensive pati ent s are not abl e to maint ai n wei ght los s and al so obese patient s are not able to achi eve and maint ai n wei ght los s through di eting al one1 0 , 2 8 , 2 9. Agai n, st ress is another possi ble expl anati on here. It has been shown that stres s is capabl e of producing changes in lipid profil e, obesit y and to elevate blood press ure.
Moreover st ress m akes us e of t he same nervous pathways as described above3 0 , 3 1.
1.9.1 Stress
Stress m a y be defi ned as al l the t ens ion, diffi culti es and obst acles wit h whi ch a pers on m ay be faced3 0. Stres s oft en im pos es demands on the indivi dual to make adj ustm ent . The res pons es to the dem and can be ver y intens e, over reac tive or adaptive. Stress ma y al so manifest as anxi et y, whi ch is a generalized feeling of fear and apprehens ion characteris ed b y the anti cipati on of danger, t ension, dist ress and arous al3 1.
A m easure of stres s i s ess enti al for effecti ve perform ance of day -to-da y activiti es of li fe, but it becom es worrisome when an i ndi vidual has exhaust ed all coping m echanis m or is mal adaptive3 0.
Stress i s m edi at ed b y t he following three s yst em s: The autonomic nervous s ys t em, the neuroendocri ne s ys tem and t he neurom uscular s ys t em.
The autonomi c nervous s yst em and the neuroendocrine s ys tems mai ntain the biochemi cal envi ronment of man withi n the limit s necessar y for opt imal
36
functioning. The neuromuscular system, on its own, mediates the individual’s external reactions3 1.
The autonomi c nervous s yst em consi sts of t he s ym pat heti c and paras ympat het ic nervous s yst ems. The sym patheti c s ys tem prepares t he bod y to fi ght and fl ee i n fri ghtful situati ons while t he paras ym patheti c s erves more localiz ed functions and is concerned with re pai r. Various chemical medi ators (or neurohorm ones ) medi at e the act ions of t he aut onomic nervous s ys t em.
The neurohormones of the s ym patheti c s yst em m ediat e energy utiliz ation whil e t hos e of the paras ympat het ic s ystem mediate energy production3 1.
The neu romuscul ar s yst em m edi at es an indi vidual ’s voluntar y and invol unt ar y reacti on to stress. Faced wi th a stres sful situati on of s uffi ci ent impact, an i ndividual ma y develop i ncreased mus cl e t one intended to bal ance the pers on for aggression or fli ght. In othe r circum st ances, the s am e indivi dual m a y los e muscul ar tone, los e bal ance and slum p down or he m a y lose tone in the urinar y bladder sphinct er and pass urine i nvol unt aril y3 1.
The sources of st ress in our environm ent i ncl ude poor li ving conditions, death of fam il y mem bers, l os s of j ob, food and s oci al ins ecurit y, frequent ph ys i cal ill nes s of fami l y members and loss of hom e through natural disast ers and wars3 0 , 3 2.
Stress ma y m ani fest itself in a number of ph ys i cal ill ness es including al coholism , obesit y, d yslipidaem ia, h yp ert ension, di abet es mellit us and/ or h yperi nsulinaemia3 1.
1.9.1.1 Alcoholis m: Alcoholism has been defined as the exces sive and com pulsi ve ingesti on and/or cravi ng for al coholi c beverage t hat oft en result s in em otional decompensati on and ph ys i cal illness3 1. It is a behaviour l argel y
37
rel at ed to st ress and the onset of al coholi sm is ass oci at ed wit h diss ati sfaction with li fe and l ow tolerance of frust ration. When a man diss atis fi ed wi th a stress ful l ife circum stance t ries to escape realit y, he t a kes al cohol, gradual l y this becom es a condi tioned reflex and a vicious ci rcle is thus creat ed whereb y the alcoholic t akes al cohol to reli eve st ress and al cohol , on the other hand, becom e a st ressor resulting in obesit y and/or h ypert ensi on depending on the severit y3 1.
Al cohol misuse has been cl ass ifi ed b y t he World Health Organisation into hazardous or harmful. Haz ardous us e is defined as a pat tern of alcohol consumption carr yi ng with it a ri sk of harm ful cons equences whi ch ma y be ph ysi cal, m ent al or soci al . Harm ful use, also call ed al cohol abuse, involves drinking t hat is alread y provoki ng eit her ph ys i cal or mental dam age but has not yet l ed t o dependence3 3. Al coholism is a known risk factor for h ypert ension3 1; haz ardous alcohol promotes wei ght gai n as it p rovides subst ant ial energy, can stimul at e appetit e and loos en rest raint1. St ress induced alcohol ism i s thus a doubl e invit ation to the ri sks of both obesit y and h ypert ension.
1.9.1.2 Ob esi ty: Some i ndi viduals when st ress ed tend to over -eat (as in bulimi a). It i s as i f the indivi dual is t r yi ng to eat his sorrow awa y. The end result is obesit y, and abnorm al li pid met abolism3 1.
1.9.1.3 Dyslipidaemia: Duri ng s tress, t he neuroendocrine s ys tem init iat es biochemi cal changes that can l ead to the mobiliz ation of fat s from fat depots and thereb y produce a h yperlipidaemi c s t at e3 1.
1.9.1.4 Hyp ertensi on: Stress is associ at ed wit h the devel opm ent of h ypert ension. This i s more so in those who have t he geneti c predispositi on.
38
During stres s, t he s ym patheti c autonom ic nervous s ys t em i s activat ed, and cert ain neurochemi cal substances are li berated. Thes e caus e a neurogenic vas oconst ri ction and a rise in blood pressure. If the stres s i s sust ained, the blood pressure can also becom e sust ained. These neurochemical subs tances can a lso ampl if y the acti on of bi ochemical subst ances that m aint ain hi gh blood pressure3 1.
1.9.1.5 Di abetes me llitus: Di abet es mel l itus i s a m et aboli c diseas e t hat has as its maj or feature, inappropri at e carboh ydrat e m et abolism . The met abolism of carboh ydrat e i s under an int ricat e hormonal bal ance. Ins ul in reduces blood gl ucos e, blood glucagon increases it. Corti sol als o pl a ys a rol e i n the ant agonism of i nsuli n actions. Under st ress , corti sol i s produced i n exces s and t ends to count er insuli n effect b y causing increas e in blood gl ucos e level b y mobilizing glucose for energy required t o cope wi th the s tress or.
Cathechol ami nes are also l iberat ed during stres s and the y als o count er ins ulin action. If the si tuati on is s ust ained, there would be a mil ieu of hi gh bl ood gl ucos e. An indivi dual prone to diabet es mell itus , and under st ress , m a y pres ent at this point3 1.
Moreover, under st ress blood gl ucos e cont rol is m ore difficult to achi eve8. Therefore more ins ulin wi ll be produced to count er the act ion of the stress neuro horm one leading to a sit uation of h yperinsuli naemi a3 1.
Thus , stres s bei ng a condition that involves a lot of neurohormones, the nervous s ys t em and the m us culoskel et al s ys t em wi th complex int erpl a y among them and other s ys t ems, can lead to obesit y and/or hy pert ens ion b y an y or al l of the m echanism s described above and possibl y b y some other
39
mechanism s yet t o be known or explained. This i s more so as it is known t hat in wom en, st ress is known to provoke l at ent illnes ses i f not well handl ed3 1.
Obesit y can caus e hypert ension through an y of thes e mechanis ms or through i nterpla y and / or combi nati on of heredit y and thes e other mechanism s. M oreover, increas es in Bod y Mass Index (BM I) have been found to correlate wel l with increas es in both s ys toli c and diastolic bl ood press ures 2 8.
Increas es in Bod y Mass Index have been ass oci at ed wit h i ncreas es i n both s ys toli c and di astoli c blood pressure. In S weden, this was found t o be so in a group of 1,462 wom en followed -up for 24 years 3 4. Als o in a group of 1,265 resi dents o f Yuexin Di stri ct of Guangzhou cit y, C hina, of those over 20 years Chines e subj ects, t he m ean s yst oli c and di astoli c bl ood pressure were found to graduall y i ncreas e wi th Bod y Mass Index, showing obvious linear rel ati ons hip between Bod y M ass Index and blood pres sure 3 5.
In Ibadan, Kadiri , et al found a correl ati on bet ween Bod y M ass Index and s ys toli c and dias tolic bl ood pressures in both men and women 3 6.