Hypertension and mental health -
It has been hypothesised that individuals with mental illness have greater blood pressure fluctuations that lead to increased cardiovascular risk and target organ damage. This systematic review aims to i investigate the association between mental illness and blood pressure variability BPV and ii describe methods of BPV measurements and analysis which may affect pattern and degree of variability.
Methods: Four electronic databases were searched from inception until The quality assessment was performed using STROBE criteria. Two authors independently screened titles, abstracts and full texts. A third author resolved any disagreements.
Whatever the cause of your high blood pressure, making healthy lifestyle changes can help manage the issue, and protect your heart and brain health. BetterHelp is an online therapy service that matches you to licensed, accredited therapists who can help with depression, anxiety, relationships, and more.
Take the assessment and get matched with a therapist in as little as 48 hours. As with the other muscles in your body, your heart will get stronger when you exercise regularly. That means your heart will be able to pump blood around your body more efficiently.
Regular aerobic activity can also help improve your cholesterol levels. If you have been diagnosed with heart disease or another serious health problem, consult your doctor before starting an exercise program.
Otherwise, to reap the heart and brain benefits of exercise, aim for:. Despite our best intentions, many of us struggle ditching our sedentary lifestyle. But there are steps you can take to make exercise less intimidating and more fun. Start small and build momentum.
If exercising for 30 minutes a day, 5 times a week sounds overwhelming, set a smaller goal and gradually build up as you gain self-confidence and momentum. Reward yourself. Once it becomes a regular habit, exercise will reward you with more energy, better sleep, a greater sense of well-being, and improved cardiovascular health.
Choose activities you enjoy. Pick activities that fit your lifestyle, abilities, and taste. See How to Start Exercising and Stick to It to learn more. The foods you eat can have a major impact on your blood pressure, not to mention your heart and brain health.
A number of different diet plans can help in controlling blood pressure, but they all feature a reduction in salt, alcohol, and refined carbohydrates , and an increase in fruit and vegetables.
The DASH diet Dietary Approaches to Stop Hypertension is a specially designed eating plan to help you lower your blood pressure.
When combined with a reduction in salt, the DASH diet can even be more effective at lowering blood pressure than medication. The Mediterranean diet emphasizes eating lots of fresh fruit and vegetables, nuts, fish, and olive oil—and only modest amounts of meat and cheese.
Following a Mediterranean diet limits your intake of refined breads, processed foods, and red meat—all factors that can help lower your blood pressure and prevent heart disease and stroke.
Limit your alcohol consumption. Drinking as little as one or two alcoholic beverages can cause a temporary spike in your blood pressure. But drinking excessively over time can greatly increase your risk of hypertension, stroke, and heart disease. Alcohol consumption can also interfere with some blood pressure medications.
Increase your potassium intake from food. Potassium can help your body get rid of excess sodium and relax blood vessels, thus helping to lower blood pressure. Bananas, oranges, broccoli, and spinach are all high in potassium.
The American Heart Association recommends no more than a teaspoon of salt a day for adults. That may sound alarmingly small, but there are many painless ways to reduce your sodium intake.
Reduce canned and processed foods. Much of the salt you eat comes from canned or processed foods like soups, convenience meals, and fast food. Cook more meals at home. Preparing your own meals gives you more control over your sodium intake.
Use fresh ingredients whenever possible and cook without salt. Use spices as alternatives to salt. Try fresh herbs like basil, thyme, or chives, or dried spices such as allspice, bay leaves, or cumin to flavor your meal without sodium.
Substitute reduced sodium versions. Choose your condiments and packaged foods carefully, looking for foods labeled sodium free, low sodium, or unsalted.
See Heart-Healthy Diet Tips to learn more. Carrying extra weight forces your heart to work harder circulating blood around your body, raising your blood pressure. The good news is that shedding pounds can have a marked impact on blood pressure.
Losing just 10 pounds could reduce your systolic blood pressure by as much as 10 mm Hg. Since our bodies are different and we respond differently to different foods, what works for one person may not necessarily work for you. To find the most effective weight loss method may take some time and experimentation with different foods and different diets.
Recognizing your emotional eating triggers and finding healthier ways to deal with stress can make all the difference to achieving a healthy weight. See How to Lose Weight and Keep It Off to learn more. While not all stress is bad for you, persistent and chronic stress can take a toll on your blood pressure and heart health.
In addition to exercise and diet, there are lots of ways you can help combat stress and bring your body and mind back into balance. Adopt a relaxation practice. Practicing a relaxation technique , such as mindfulness meditation, progressive muscle relaxation, or deep breathing can elicit the relaxation response, a state of deep rest that puts the brakes on stress, slows your breathing and heart rate, and lowers your blood pressure.
Talk to a trusted friend. Nothing eases stress more effectively than chatting face-to-face with a friend or loved one. Make time to connect with the people closest to you. Get enough sleep. You can break the cycle and ensure you get enough quality sleep at night by modifying your daytime habits and developing a peaceful bedtime routine.
See Stress Management to learn more. The nicotine in tobacco causes your body to release adrenaline that stimulates your nervous system and forces your heart to work harder to circulate blood.
Nicotine can also interfere with certain blood pressure medications. While quitting is never easy, once you stop your body will benefit from improved circulation almost immediately. But it can be done. See How to Quit Smoking to learn more. While some people may only need to work on one or two areas to reduce their blood pressure—getting more exercise or quitting smoking, for example—most of us find that we need to improve our habits in at least 3 or 4 areas.
Making lots of different lifestyle changes at the same time can be overwhelming. Start gradually and make one or two changes to begin with. Once those changes have become habit, you can tackle one or two more, and so on.
For example, you may decide to start by giving up smoking—and adopting some relaxation techniques to help with the stress of quitting—then move on to losing weight or improving your diet.
Lose the all or nothing thinking. Doing something, no matter how small, is always better than doing nothing.
Set specific goals. The more specific your goal, the easier it is to stick to. Make a plan. We therefore investigated the effect of blood pressure variations on emotional task-based functional MRI activation 31 , Overall, there were data of , participants , [ The final sample size for each analysis after exclusion of missing data is reported in the respective results sections below.
Our study included UK Biobank data i from the complete baseline assessment, which was conducted between —, and ii from the ongoing year follow-up visit which has started in and included brain magnetic resonance imaging MRI. Our follow-up visit sample consisted of those participants whose data had been released by February In addition, a sub-sample of the baseline cohort participated in an online mental health follow-up assessment in We defined mental health variables depressive symptoms, well-being at baseline and follow-up as outcomes.
Systolic blood pressure SBP , hypertension diagnosis HTN , and number of prescribed antihypertensive medications at baseline and follow-up were the main predictors in all models.
Finally, we assessed the relationship of the main predictors with emotion-related brain function i. As shown in Table 1 , participants with and without HTN diagnosis differed with respect to all descriptive variables at initial assessment.
Missing data were evident in all variables of interest with varying impact SBP 45, [9. At follow-up assessment, missing data were evident for SBP 11, [ Missing data were listwise excluded and all following analyses conducted on complete-case datasets.
To account for bias due to missing data, we imputed data and conducted sensitivity analyses on the entire sample, which are reported below and in Supplementary Table 5. The results from imputed datasets indicated no sign of bias due to missing data and replicated our results from complete-case analyses Supplementary Table 5.
At initial assessment, self-reported current depressive symptoms resulted in a mean score of 1. At follow-up, depressive symptoms were reported with mean score of 1. Thus, test-retest reliability of mood assessments was high, indicating stability over assessment timepoints.
For the multiple linear regression testing cross-sectional associations of SBP, HTN, and number of antihypertensive medications with depressive symptoms , participants could be included in the model, while , could be included for the multiple linear regression model with well-being as outcome.
At baseline Fig. Source data are provided as a Source Data file. Overall, the model for depressive symptoms including all participants yielded a model fit of adj.
For the multiple linear regression testing longitudinal associations of SBP, HTN, and number of antihypertensive medications with depressive symptoms 28, participants could be included in the model, while 29, could be included for the multiple linear regression model with well-being as outcome.
Longitudinally Fig. Next, we explored if the relationship between mental health and SBP was moderated by hypertension status at follow-up assessment. First, we excluded participants who were hypertensive at the initial assessment defined as HTN diagnosis or intake of antihypertensives. Across all participants, SBP increased from initial assessment to follow-up Fig.
People who later developed HTN already had higher SBP levels at initial assessment compared to people who stayed normotensive Fig.
Notably, in unadjusted models, there were no significant group differences in mental health at initial assessment between people who developed HTN and those who stayed normotensive Fig. However, in the fully adjusted regression model, we observed a main effect of later HTN on baseline mental health Fig.
The regression model further yielded a significant interaction of SBP at initial assessment and HTN at follow-up with depressive symptoms at initial assessment, showing that the association between SBP and depressive symptoms was moderated by hypertension status at follow-up Fig.
Thus, the slope of the relationship between higher SBP and fewer depressive symptoms was steeper in those participants who developed HTN approximately 10 years later. Similarly, a trend of a moderation by HTN status was observed for the association between well-being and SBP at initial assessment, but this effect was not significant Fig.
B People who developed hypertension until follow-up i. E Participants who developed hypertension dark blue colour had a steeper negative slope for the relationship between blood pressure and depressive symptoms than those participants who stayed non-hypertensive light blue colour.
F Similar trend for well-being in the expected opposite direction. This resulted in a sample where the two groups had SBP levels in the normotensive range at baseline. The results within this sample remained virtually unchanged and are reported in detail in the Supplementary Results.
To explore a central nervous representation of emotional reactivity, we assessed how hypertension status relates to emotional processing in the brain using fMRI activity assessed during the Hariri task. We repeated the same analysis using the blood pressure measurement at initial assessment which was acquired ~10 years prior to neuroimaging and thus not directly related to blood flow and volume dependent effects during BOLD fMRI.
Interestingly, already the baseline SBP i. The colour gradient represents the density of data points. Right column shows the same, but grouped by HTN at follow-up. Dark blue colours represent people who became hypertensive from baseline to follow-up.
Light blue colours represent participants who stayed normotensive. The negative correlation between systolic blood pressure and emotion-related activity was flattened in participants who had developed hypertension.
We performed several additional and sensitivity analyses to test the robustness of these results. Moreover, sensitivity analyses were performed to test whether the above reported confirmatory results were dependent on vii the presence or absence of previous diagnosis of depression or any other severe disease that might affect BP list of diseases in Supplementary Table 2 ; viii the intake of antidepressants or any other medication intake; ix a specific effect of certain antidepressant or antihypertensive drug classes.
Finally, we x performed multiple imputation of missing data, xi assessed potential survival bias, xii explored potential unmeasured confounding effects with E-values, and xiii applied joint modelling of time-varying effects of SBP and HTN using Linear Mixed Effects Models. The results of all additional and sensitivity analyses are reported below and in the Supplementary Materials.
In sum, the results were overall robust and consistent: independent of any potential confounders including medication intake, there was an effect of higher SBP on fewer depressive symptoms and higher well-being, as well as a negative effect of HTN diagnosis on mental health. Number of antihypertensive medications at baseline was not significantly associated with the PHQ-9 depression score.
The results from the PHQ-9 highly resemble the results using the depression score reported in the main manuscript Supplementary Fig 4. We further analysed cross-sectional models at both follow-up time points. For the number of antihypertensive medications, we observed significant associations with all mental health outcomes, suggesting that higher hypertension burden, indicated by a higher number of prescribed antihypertensives, negatively relates to mood.
We additionally evaluated how the association between SBP and depression presents in varying quantiles along the range of SBP levels, similar to previous studies 33 , 34 , Next, we computed the cross-sectional association between SBP bins and depressive symptoms at baseline while adjusting for the same covariates as in the main manuscript.
We also included the UK Biobank assessment centre to model that data acquired at the same assessment centre might be correlated. Among these additionally included covariates Supplementary Fig 7 , insomnia had the largest effect i.
While all other additionally included covariates also had some effect on mental health, the effects of our main variables of interest SBP, HTN, No. of antihypertensives on both mental health outcomes remained virtually unchanged when controlling for all these confounders.
To complement our results using self-report data with clinical assessments, we repeated the confirmatory analyses using hospital diagnoses for HTN and depression from the HES database. We used the secondary ICD diagnoses codes a participant has had recorded across all their hospital inpatient records Supplementary Table 1.
The occurrences were summed per participant and coded as 0 or 1 for the absence or presence of HTN or depression, respectively. Including HES-diagnosed HTN instead of self-reported HTN replicated our main results Supplementary Fig 8. The results yielded larger effect size estimates i.
Overall, the models including HES HTN explained slightly more variance, as reflected in greater adjusted R 2 -values compared to the models using self-report HTN depressive symptoms: adj. The overall model fit was low adj.
In the moderation analysis Fig. We therefore refined our criteria to thoroughly detect all hypertensive participants at both initial assessment for conservative exclusion and at follow-up to clearly define who will develop hypertension.
However, in the fully adjusted regression model e. The moderation was however not significant for depressive symptoms at follow-up.
Neither did we observe any significant moderation effects of developing HTN for well-being at any of the assessments. In sum, these results corroborate our findings that people who developed HTN throughout the course of the study might require higher SBP levels to sustain the same mental health outcomes as normotensives and that the negative relationship between mental health and blood pressure was accentuated in people developing HTN several years before HTN manifested.
We also tested if any effects of SBP, HTN and antihypertensive intake on current depressive symptoms and well-being depended on the presence or absence of previous diagnosis of depression or any other severe neurological, systemic, or psychiatric diseases that might affect BP e. We thus performed the same multiple linear regression models described above separately for groups of participants with or without any of these diseases.
As described in Supplementary Table 3 , in people both with or without depression diagnosis, SBP was negatively associated with depressive symptoms and positively with well-being.
Inversely, in both sub-groups HTN was positively related with depressive symptoms and negatively with well-being. Higher intake of antihypertensives was related to fewer depressive symptoms only in people without previous depression.
The results were also robust in sub-samples of people without or with diseases which often co-occur with changes in blood pressure, such as cardiovascular or renal diseases Supplementary Table 3. Only number of antihypertensives yielded diverging results between these sub-groups: While people without disease diagnoses, showed a negative association between number of antihypertensives and depressive symptoms and a positive one with well-being scores, higher intake of antihypertensives was related to more depressive symptoms and lower well-being in people with any diseases Supplementary Table 3.
Among the most frequently used medications were pain killers e. We therefore explored potential effects of these medications on the cross-sectional relationship between blood pressure and mental health at baseline. Again, in separate multiple regression models of groups of participants taking or not taking these medications, we added SBP, HTN and number of antihypertensive medications simultaneously as predictors of depressive symptoms and well-being and corrected the models with the same covariates as described in the confirmatory analyses above.
Sub-group analyses of participants taking or not taking antidepressant medication, showed similar associations between SBP, HTN and mental health as analyses on the total sample Supplementary Table 4.
We also compared the blood pressure-mental health relationship between participants taking any sort of medications and those who took none Supplementary Table 4. Again, we found a negative effect of SBP and a positive effect of HTN on depressive symptoms and the inverse pattern for well-being in both sub-groups Supplementary Table 4.
Despite the smaller sample sizes, standardized beta estimates were slightly larger for the sub-group of participants who did not take any medications, compared to the total sample Supplementary Table 4 and Fig. In addition, we tested whether there was a specific effect of antidepressant or antihypertensive drug classes on the relationship of blood pressure and mental health see Supplementary Fig 2 and 3 for list of medication classes.
For these analyses, we categorised antidepressants and antihypertensives according to their mechanisms of action. In separate multiple regression models, we added SBP, HTN and a categorical variable coding for the medication classes simultaneously as predictors of depressive symptoms and well-being and corrected the models with the same covariates as described in the confirmatory analyses above.
To account for bias due to missing data, we imputed data and conducted sensitivity analyses on the entire sample. Analyses reported above were based on the complete-case data with listwise exclusion of missing values, and the cross-sectional models at baseline assessment were repeated in imputed data for comparison.
To impute datasets, we created 20 imputations using multiple imputation by chained equations with the R package MICE version 3. The non-surviving sample was older, had higher blood pressure and reported more diagnoses than the total sample Supplementary Table 6.
Overall, the models in the non-surviving sample explained slightly more variance, as reflected in greater adjusted R 2 -values compared to the models in the surviving sample depressive symptoms: adj.
To also explore the effect of potential unmeasured confounders on the results, we calculated E-values using the EValue package in R version 4. E-values indicate the minimum strength of association, on the risk ratio scale, that an unmeasured confounder would need to have with both the exposure and outcome to explain away an exposure—outcome association, above and beyond the measured covariates.
For continuous exposure variables, such as SBP in our study, the function uses a dichotomisation in the exposure between hypothetical groups of participants per one-unit increase.
For the continuous outcome, such as depressive symptoms and well-being in our study, the function uses an effect-size conversion to approximately convert the mean difference between the exposure groups to the odds ratio that would arise from dichotomising the continuous outcome The interpretation of the E-value depends on the context regarding the measured confounders.
Given that we have included several plausible confounders in our models, the resulting E-values give further support for the robustness of our results, as an unmeasured confounder would need to be associated with outcome and exposure by a risk ratio of around 1.
However, we also note that while E-values have been introduced as robustness analyses for studies aiming to estimate causal effects 46 , we consider them an additional sensitivity measure for robustness. Potential causal effects should more directly be investigated in future studies with experimental designs or observational designs with dedicated causal identification strategies e.
Separate models were set up for depressive symptoms and well-being as outcomes, respectively. Each full model was compared to a null model that was identical but did not include the interactions. Chi-squared values and p-values for each interaction effect were derived by dropping interactions iteratively reduced models.
Non-significant interactions were dropped from the full model to yield a less complex reduced model. The significant interaction of SBP and time point indicates that the relationship between SBP and depressive symptoms changes between assessments.
Evaluation of the fixed effects revealed that the interaction was driven by a steeper negative slope at baseline than at follow-up. The stronger negative relationship between SBP and depressive symptoms at baseline compared to follow-up supports our observation from multiple linear regression analyses showing that the relationship was stronger for the cross-sectional analysis at baseline than for the longitudinal analysis including follow-up outcomes.
No significant difference between individuals with and without HTN was found regarding the relationship between SBP and depressive symptoms across both time points i.
This observation is in line with the results from the moderation analysis, which showed a moderating effect of impending HTN on the relationship between SBP and depressive symptoms at baseline assessment, but not at follow-up.
With these additional mixed model analyses, we were able to include all available data including participants with missing data; confirming the findings from multiple linear regression models reported in the main manuscript.
In this study, we confirmed two seemingly contradictory associations of high blood pressure with mental health: i Higher SBP was associated with fewer depressive symptoms and greater well-being at the initial exam as well as at the 5-year mental health online follow-up and the year follow-up including imaging, whereas ii the presence of a HTN diagnosis was associated with more depressive symptoms and lower well-being.
Given the well-powered cohort of the UK Biobank, we were able to perform sensitivity analyses which confirmed that the observed associations were robust to biases of medications e.
Strikingly, we furthermore found that iii already at the initial exam, among normotensive individuals, mental health was negatively affected more depressive symptoms, lower well-being by the later HTN status at 10y-follow-up. Also, iv the relationship between blood pressure and mental health — at the initial exam — was moderated by later HTN, such that the negative association between blood pressure and depressive symptoms was stronger in those participants who later developed HTN.
Finally, v our results from task-based functional brain imaging provide further support for an impact of blood pressure and HTN on central processing of emotions: We demonstrate a negative relationship between SBP — at baseline ~10 years prior to fMRI and at the time point of imaging — and the BOLD fMRI response to aversive emotional stimuli.
This relationship was again moderated by HTN status at follow-up, such that people who developed HTN showed overall lower responses to aversive stimuli and a flattened negative relationship between SBP and brain responses.
Taken together, our results support the notion that the interrelation between blood pressure and mental health may be involved in the development of high blood pressure with potential implications for developing new preventive and therapeutic approaches for essential hypertension. We preregistered and confirmed a conceptional replication that higher SBP related to better mood ratings: Our findings are consistent with studies reporting positive effects of elevated blood pressure on mental health, including decreased depressive symptoms 16 , 17 , 18 , better quality of life 12 , 18 , and reduced self-reported stress 13 , 14 , We extend these findings, which were based on either cross-sectional designs or shorter follow-up periods years , by demonstrating that baseline SBP remained a significant predictor of mental health up to 10 years later.
The positive effects of high blood pressure on mood might be related to research findings showing that higher blood pressure diminishes emotional experience in experimental manipulations 47 , 48 , It is also well established that elevated blood pressure robustly reduces the perception of physical pain 21 , 25 , 50 , 51 , but also social pain It has therefore been hypothesised that elevated blood pressure relates to a generalised attenuation of emotional valence processing 25 , Our fMRI findings are consistent with this notion, suggesting an impact of blood pressure on the processing of negative emotional faces, even at a follow-up after 10 years.
Importantly, while affective attenuation might relate to coping mechanisms to lift mood in stressful situations, it could reinforce staying in potentially harmful circumstances over prolonged periods of time. This may lead to further blood pressure increases and eventually to HTN see below 20 , 25 , 27 , 28 , Given these consistent findings of a positive association between blood pressure and mood, it seems paradoxical that we found a different pattern for diagnosed HTN; albeit again in line with previous studies in which the presence of vascular risk factors or manifest CVD has been associated with increased depressive symptoms 53 , 54 and decreased well-being Several potential explanations have been put forward: Biological explanations build on well-known pathophysiological consequences of chronic blood pressure elevations e.
leading to ischaemic brain damage indicated by white matter lesions, microinfarcts, and cerebral micro-haemorrhages White matter lesions, in particular, have been linked to the occurrence of depression with a vascular component 57 , Systemic mechanisms resulting from unfavourable metabolic alterations, which are common in people with HTN, and an unhealthy lifestyle e.
have also been linked to depression via metabolic, immuno-inflammatory, and autonomic pathways reviewed in Psychological explanations, on the other hand, emphasise that individuals receiving a diagnosis of HTN are often confronted with a sudden awareness of a chronic illness that requires medical attention and a change of lifestyle.
The negative psychological consequences of such a labelling effect could underlie opposing effects of elevated blood pressure and HTN diagnosis on mental health 60 , Based on our data, we cannot exclude contributions of the factors discussed above, however, a major finding of our study i.
Yet, in the fully adjusted model, i. In both analyses — when unadjusted for blood pressure — there were no significant differences in mental health at either visit, while the difference was highly significant when adjusted for blood pressure. Interestingly, we also noted in both analyses that the two groups differed regarding the overall mood-lifting effect of higher blood pressure at the initial visit, such that this effect was more pronounced in the group of those participants who developed HTN later.
Thus, it seems that in the HTN-developing group, the relationship between blood pressure and mental health was both shifted in magnitude and had a different slope. This finding cannot be explained by the labelling effect and is also unlikely to be related to vascular damage, such as white matter lesions, as these occur only after long-lasting blood pressure elevations.
Obvious candidates for explaining effects of blood pressure on mental health are regulatory circuits linking arterial blood pressure to central processing in the brain.
While the causal, and likely multifactorial, pathways between blood pressure and mental health are not fully understood, a shared mechanism between subjective experience, emotional processing and pain involves the regulatory baroreflex system.
Baroreceptors, stretch sensitive receptors located in the aortic arch and the carotid artery sinus, are the peripheral sensors of blood pressure 62 , 63 , During each heartbeat, baroreceptors are activated during systole and become less active during diastole.
They are known to relay phasic and tonic information about blood pressure via the vagal and glossopharyngeal nerves to brain stem nuclei which orchestrate adjustments of blood pressure and heart frequency via the parasympathetic and sympathetic nervous system 62 , 63 , Importantly, in addition to their role in adjusting blood pressure and heart frequency, baroreceptor activation has also been shown to influence emotional and pain processing reviewed by Suarez-Roca et al.
Direct evidence comes from animal studies, in which for example, pain-relieving effects of blood pressure elevations were abolished by baroreceptor denervation 20 , 27 and from studies in humans in whom local baroreceptor stimulation modulated pain perception 21 , 24 , 25 , Further evidence has been provided by numerous studies showing different processing of pain, emotion, and sensory stimuli in systole versus diastole 22 , 23 , 26 , Importantly, it is also well established that the development of HTN is characterised by a progressive desensitisation of baroreceptors and altered sensory processing 27 , It, therefore, seems highly plausible that relatively reduced baroreceptor signalling might also underlie the observed altered relationship between blood pressure and mental health in hypertensive people.
Our results furthermore indicate that the altered relationship between blood pressure and mental health may already be present years before the diagnosis of HTN. In a similar vein, our fMRI findings show an altered relationship between blood pressure and BOLD activation to negative facial expressions in people with HTN, consistent with adjusting central processing of emotions as a response to baroreceptor desensitisation.
In sum, there is evidence that baroreceptor signalling can underlie the effect of higher blood pressure on mental health. With regard to the development of blood pressure increases over the life course and eventually the pathophysiology of arterial HTN, our findings are consistent with the notion of feedback loops wherein arousing emotional stimuli and stressors elevate blood pressure, which in turn activates baroreceptor pathways that induce analgesia and decrease the perceived affective magnitude of a stressor While psychosocial stress is increasingly accepted as a risk factor for the development of hypertension 67 , blood pressure adjustments — via baroreceptor signalling — may link stress to a rewarding mechanism decreasing perceived stress.
Reinforcement by repeated stress exposure may eventually lead or contribute to increases in blood pressure and the development of essential HTN 20 , 25 , 27 , 28 , Our data further emphasise inter-individual differences: Those individuals who later developed HTN on average showed lower mental health scores when adjusting for SBP.
In addition, our moderation analysis yielded that the development of HTN was associated with a stronger negative correlation between mental health and blood pressure at baseline, years before the HTN diagnosis.
While the observed inter -individual differences cannot be readily interpreted as indicative of intra -individual mechanisms, it is nevertheless tempting to speculate that people at higher risk of developing HTN require higher blood pressure levels to sustain the same mental health outcomes.
These individuals may find themselves on a relatively steeper trajectory towards HTN due to the stronger mood-lifting effect of blood pressure increases.
Taken together we propose that i feedback loops between blood pressure and rewarding emotional processing during periods of stress may play a role in the pathophysiology of blood pressure increases and HTN and that ii alterations of these feedback loops characterised by a shifted blood pressure - mental health relationship may increase HTN risk in affected individuals.
Based on our data, we cannot differentiate between potential reasons for the altered blood pressure-mental health relationship in the mostly middle-aged participants, which may include genetics, life-style factors, such as nutrition or the environment, previous exposure to acute and chronic stress, or other factors.
Clearly, there is a need for prospective longitudinal studies clarifying this issue. Beyond effects of blood pressure and diagnosed HTN, other factors such as medication and previous diseases can influence mental health and thus be confounders in our analyses.
For example, Hermann-Lingen et al. Boal et al. Additionally, intake of antidepressant drugs has been previously related to elevated blood pressure To account for these potentially confounding factors, we investigated effects of the presence or absence of a lifetime major depression diagnosis, other forms of chronic illness as well as intake of antihypertensive medications in sensitivity analyses.
Importantly, the findings of our study were robust and consistent: Independent of any potential confounders including medication intake, there was a mood-lifting effect of higher SBP on depressive symptoms and well-being, as well as a negative effect of HTN diagnosis on mood.
The results reported here are contingent on several limitations. We used UK Biobank data which is not representative of the middle-aged and older UK population The sample, particularly the neuroimaging sub-sample, displays the healthy volunteer effect, which describes that UK Biobank participants are considered to be more health-conscious, self-reported fewer health conditions and show lower rates of all-cause mortality and total cancer incidence compared to the general population Yet, associations between risk factors and disease outcomes in UK Biobank have been reported to be generalisable despite the healthy volunteer effect 69 , Similar to previous studies, we used self-reports of HTN and antihypertensive medications.
Self-reported HTN can underestimate the true underlying prevalence 71 and may influence subjective health itself In addition to self-report measures, we included direct standardised blood pressure recordings, as well as Likert-scale measures of depressive symptoms and well-being, which enabled us to parametrically model these exposures and outcomes in linear regression models.
A recent study also showed that averaging blood pressure values from the first and second reading, as we did here, might underestimate the true prevalence of HTN While we have not used the blood pressure readings to define HTN in our study, we acknowledge that the procedure of blood pressure readings may have an undetected effect on our results.
Yet, our results converge also when using HTN diagnosis from self-reports and hospital records, which strengthens the overall confidence in the robustness of our findings. Conceptually, one may question the strict dichotomy between HTN versus no HTN, particularly as blood pressure thresholds for HTN diagnosis have shifted towards lower values in the last decades.
However, given the diagnostic criteria for HTN at the time of the study, we assume them to be followed by most physicians in clinical care.
Thus, we consider the self-reported HTN status to be a reasonable definition with predictive value for clinical outcomes in an epidemiological study Based on our preregistered hypotheses, we only tested linear associations between blood pressure and mental health.
While Montano 16 showed that non-linear models testing cross-sectional blood pressure-mood associations do not outperform linear models, longitudinal trajectories of both blood pressure, mental health and their interaction over the lifespan are plausible and may reveal diverging patterns.
Thus, no direct conclusion can be drawn from our observations relevant for individual patient care. Given the known effects of blood pressure on emotional processing, we hypothesise that —despite the small inter-individual effect sizes in our study — more pronounced intra-individual effects might exist.
Our study may motivate future work testing the hypothesis that blood pressure variations and associated mental health need to be taken into account, also in the individual management of people at risk for HTN.
Future studies should also address the point of potential practical implications for treating high blood pressure in severe clinical depression. Considering the high prevalence of HTN and its treatment in the general population, as well as rising numbers of sub-clinically elevated blood pressure, small effect sizes may be epidemiologically relevant.
Our fMRI findings may be confounded by alterations in neurovascular coupling with HTN While this should be largely accounted for by reporting the BOLD activation contrast between two different types of stimuli emotional faces versus shapes , we cannot exclude the remaining impact of impaired neurovascular coupling.
Since the Hariri-task was limited to faces with negative emotions, future studies may add information about the impact of blood pressure on the neural processing of positive emotions. Importantly, our results are not ideal to draw firm conclusions about the causality and directionality of the associations between blood pressure, HTN, and mental health, particularly the differentiation between effects of blood pressure per se and HTN remaining complex.
Finally, randomised controlled trials targeted at assessing the bi-directional relationships of blood pressure and mental health will provide strong designs to elucidate these effects. In summary, in a large British population sample of generally healthy middle-aged and older individuals, we found a relationship of elevated blood pressure with fewer depressive symptoms and greater well-being extending to a follow-up period up to around 10 years.
We found the opposite effect for diagnosed HTN — already years before the timepoint of diagnosis. Participants who were normotensive at baseline and later developed HTN showed alterations in the blood pressure-mental health relationship already at baseline.
An additional strength of our study lies in the use of fMRI analyses, which suggested an impact of blood pressure levels and HTN development on the neural processing of emotional stimuli. The results were overall robust to bias of medications, chronic illness, survival, social factors, and unmeasured confounds.
While the observed effects are small and results from this observational study may not be directly applicable to clinical outcomes, our study adds perspective on how the interrelation of sub-clinical mental health and blood pressure might be involved in blood pressure increases during ageing and development of HTN that could have implications for developing new preventive and therapeutic approaches.
All participants gave written informed consent. This approval means that researchers do not require separate ethical clearance and can operate under the Research Tissue Bank RTB approval. All analyses and data visualisations were performed with R 4.
The UK Biobank is a publicly available, on-going longitudinal study that aims to comprehensively assess the health-related indices of more than , UK citizens UK Biobank included participants from the UK between the ages of 40 and 69 years at recruitment in to The size of the cohort was determined based on statistical power calculations for nested case-control studies to achieve large incidences and reliable odds ratios of common health-related conditions during the first years of the years follow-up period The initial assessment of the whole cohort was conducted between in 22 assessment centres throughout the UK.
The complete assessment protocol was repeated at two other instances, specifically at first repeat assessment visit , and at imaging follow-up which included ongoing brain magnetic resonance imaging MRI assessments of , UK Biobank participants that has started in 75 , A set of questions and measures designed for the assessment of current and lifetime mental health and psychosocial factors were administered at several instances during UK Biobank data acquisition 40 , 77 , For this study, we used data from the initial assessment visit i.
The following variables were included in this study details on the UK Biobank data fields that were used for each variable are reported in Supplementary Table 1. Current depressive symptoms: During each assessment centre visit, frequency of current depressive symptoms in the last two weeks i.
The item scores were summarized as mean scores for the purpose of this study. Questions regarding current depressive symptoms were assessed via a touchscreen during baseline and follow-up assessment centre visits 40 , 77 , We also preregistered analyses using the Patient Health Questionnaire 9-question version PHQ-9 79 from the online mental health follow-up assessment which a sub-sample of the whole UK Biobank cohort received In the online PHQ-9 questionnaire, the severity of current depressive symptoms in the last two weeks was assessed.
Since UK Biobank applied a different coding scheme, the items were recoded to match the original coding as described above. PHQ-9 symptom scores were summarized as a sum score. The analyses and results of this questionnaire were almost identical to the ones obtained from the main depressive symptoms outcome measure described above.
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High Blood Pressure, Cardiovascular Disease and Mental Health - What's the Connection? Hypertension and mental health is Energy management techniques for athletes known that the rise and fluctuation of blood Hypertension and mental health are closely related to mood and ad. In addition to physical halth, psychosocial factors play an important role mentap the pathogenesis of hypertension. Long-term depression, insomnia, stress, anxiety, or sharp and intense trauma are also important causes of hypertension as research suggested. To pay full attention to the relationship between hypertension and mental health status and to identify and give effective psychological, social, and drug intervention in mental and psychological disorders and hypertension caused by it at an early stage is helpful to further improve the level of prevention and treatment of hypertension. It is of great significance to improve the prognosis.BioMedical Hwalth OnLine volume 21Article number: 19 Cite this article. Healthh details. Mental illness represents a major global burden healthh disease Hypdrtension. It has been hypothesised that individuals with mental Gamer fuel refill have greater blood heaalth fluctuations that Hypertensipn to increased cardiovascular risk and target organ haelth.
This systematic review aims to i investigate the association between mental Coenzyme Q and fertility and blood pressure variability BPV and Hypertension and mental health heallth methods of BPV measurements Hypertensipn analysis which may affect pattern and degree of variability.
Four electronic databases were searched from inception until The quality Hyperetnsion was performed znd STROBE criteria. Two authors independently screened titles, abstracts and full texts. A third author Hypertensionn any disagreements.
Hypeetension studies met the inclusion criteria. Three studies measured short-term BPV, two Chromium browser for media streaming long-term BPV and seven mentql ultra-short-term BPV.
Hyperrtension studies related to Hypertemsion BPV using ambulatory Hypertension and mental health Hydration for staying hydrated during exercise blood pressure monitoring found a Responsibly Harvested Produce BPV in individuals with depression or panic disorder.
The two studies measuring long-term BPV were mentwl to the Hypertension and mental health population Maintaining glucose levels found mixed results. Mental illness is significantly associated with menttal increased BPV in younger and middle-aged adults.
All studies of ultra-short-term BPV using standard cardiac autonomic assessment; non-invasive continuous finger Gut health and gluten intolerance pressure and heart rate Hyppertension found significant association between BPV and Hyppertension illness.
A mixed result related to Type diabetes heart health of tilt during tilt assessment and between controlled Hypertwnsion spontaneous breathing were observed mntal patients with Hypetrension state. Current review found that people with mental illness is Antioxidant supplements for eye health associated with an increased BPV regardless Hypertensiion age.
Since mental illness menral contribute to the deterioration of autonomic function HRV, BPVearly therapeutic intervention in mental illness may prevent diseases associated with mentzl Hypertension and mental health and reduce the likelihood of negative cardiac Hypertensiom.
Therefore, these findings may have important implications for patients' future physical health EGCG and caffeine well-being, highlighting the need for comprehensive cardiovascular risk reduction.
Mental illness, such as an, depression and bipolar disorder, poses a significant global Hypertensionn burden [ 64 ].
The presence of mental illness is associated with increased morbidity and mortality [ 36 ]. Cardiovascular disease is the most mmental cause of death Hypdrtension individuals with mental illness [ 1536mmental ].
Yealth led to Reduce sugar consumption hypothesis that individuals Hyperrension mental illness Essential oils for pain relief greater blood pressure fluctuations resulting in increased cardiovascular risk and target healfh damage Hyoertension 3640 ].
Impaired Menatl function, healty reflected in both sympathetic and parasympathetic activity of the autonomic nervous system, is associated Hypertension and mental health an increased risk of cardiovascular Hyperteension [ 14 ].
Conventional methods to assess menyal function include Nutrient absorption rate of heart rate and blood pressure changes in response to a series Sleep and nutrition for athletes challenge manoeuvers.
These methods are relatively crude and lack sensitivity, and therefore not routinely used in practice [ 11 ]. Newer methods of measuring heart rate and blood pressure changes include measurement of Hypertension and mental health rate variability HRV and blood pressure helth BPV.
These mmental require minimal patient cooperation hwalth have a high level of sensitivity. HRV is an assessment of beat-to-beat variation in the heart, Hyertension is increasingly used because it is menttal to measure and is a hfalth indicator for autonomic function [ 440 ].
Based on studies on heart rate estimation, mengal ECG signals will first undergo a pre-processing emntal that includes denoising, segmentation, and filtering to remove any undesirable noise Hyperetnsion artefacts [ 49 ].
The other purpose of filtering is to emphasise the heartbeat peaks QRS an of the ECG signals so that amd distance between consecutive peaks can be measured i. each R peak corresponds to anv heartbeat [ 51 ]. Heart rate Hgpertension heart rate variability values can be estimated abd these steps are completed.
A review Hypertensikn heart heakth variability and Shortness of breath suggested Hypertenssion a constantly changing heart rate is a sign of healthy regulatory systems that can successfully adjust to environmental and psychological ehalth [ 47 ].
Reduced Hyperetnsion, on Grilled vegetable skewers other Hy;ertension, indicates that the body's stress response is not optimal, potentially exacerbating the negative Hypertension and mental health of ajd stress and increasing the risk of stress-related medical conditions.
Menhal studies Hypertensioon that HRV indices, as provided by telemedicine Hypertension and mental health remote healthcare adn [ 51 ] were significantly reduced in patients with depression [ 31 Skincare for dark spots, 53 ] and anxiety disorders, including generalised anxiety disorder Inflammation and respiratory healthsocial Pomegranate extract benefits disorder, panic disorder and Hypertendion stress disorder Hypertenaion 1632 ].
Thus, we can conclude from a number of studies on HRV and mental illness that lower HRV in patients with mental illness is associated with poorer cardiovascular health outcomes and a variety of vascular diseases [ 2 ]. On the other hand, BPV refers to fluctuations in blood pressure that occur within several minutes, over a h period or a longer period of time several years [ 45 ].
While blood pressure fluctuations over a h period are normally obtained using non-invasive ambulatory blood pressure recorders, continuous, beat-to-beat blood pressure measurements are acquired using the photoplethysmographic PPG technique.
Long-term BPV has been associated with stroke and coronary events in high-risks patients [ 55 ], while visit-to-visit short-term BPV is a prognostic indicator for cardiovascular mortality in patients with hypertension [ 44 ].
Although the association between BPV and coronary diseases has been widely reported, the mechanisms linking these two are unclear due to the dynamic nature of blood pressure, which fluctuates with environmental stimulations and daily life challenges [ 4446 ].
According to Parati et al. While BPV has been widely studied in hypertension [ 3462 ], less is known about its relationship with mental illness.
Several studies have reported an increase in BPV in individuals with mental illness, which has been linked to an increase in their cardiovascular risk and target organ damage.
However, conflicting findings with regard to BPV in patients with psychological disorders have been reported. This may be caused by inconsistencies in the study design among different clinical studies, measurement techniques and experimental procedures as well as types of BPV analysis.
Therefore, the current systematic review aims to i investigate the association between mental illness and BPV; and ii provide an in-depth analysis on the study design, blood pressure BP measurement techniques and assessment intervals as well as types of BPV indices used in each study.
This would help improve the design of future clinical trials, which aim to identify the relationship between BPV and psychological disorders and use BPV as early indicators of cardiovascular diseases in these patients.
Figure 1 shows the study identification and selection process. Of the records identified through database searching and through other sources, studies were potentially eligible after removal of duplicates.
Following screening of title, abstract and full-text articles, 12 articles fulfilled the inclusion criteria. Flowchart of the study identification and selection process. BPV blood pressure variability. The majority of the studies provided detailed information about the research framework.
Eleven studies provided a clear description of background of study, aims, objectives and hypotheses in the introduction. No studies reported the sample size calculation, and only two studies addressed missing data [ 5765 ].
Table 2 summarises the characteristics of the 12 studies. Five studies involved older adults aged 55 years and above [ 4148565759 ], whilst the remaining seven studies assessed BPV in the younger to middle-aged population aged 18 to 46 years [ 16713356165 ].
All studies included both males and females [ 6134156575965 ]. The presence and severity of mental health symptoms or the diagnoses of mental illness was assessed using a number of validated assessments or tools.
The assessment tools and the methods of diagnoses are listed in Table 2. Of the 12 included studies, three aimed at gaining additional insights into the psychological state using the short-term BPV analysis method [ 1741 ].
Alici et al. The third study [ 41 ] identified subjects with depression using the item Depression rating scale through a self-administered questionnaire. Both long-term BPV studies identified patients with late-onset depression [ 56 ], generalised anxiety disorder and depression disorder [ 57 ] using the MINI International Neuropsychiatric Interview MINI screening tool.
The interviews were conducted face-to-face by trained clinical psychologists [ 56 ]. Of the seven ultra-short-term BPV studies, four involved psychiatrists to diagnose psychological disorders, and trained clinical interviewers to administer structured clinical interviews with DSM-III-R Diagnostic and Statistical Manual of Mental Disorders, third addition, revised [ 63565 ] and DSM-IV.
Another study [ 13 ] performed face-to-face structured clinical interviews based on the MINI International Neuropsychiatric Interview screening tool to identify patients with major depressive disorder. Lastly, self-reported questionnaires, which include Brief Symptoms Inventory BSISpielberger State—Trait Anger Expression Inventory STAXI and Toronto Alexithymia scale TASwere administered by trained researchers in the study by Virtanen et al.
A number of physiological assessments were used to determine the HRV and BPV. Studies which measured short-term BPV [ 1741 ] and long-term BPV [ 5657 ] utilised either Ambulatory Blood Pressure Monitoring ABPM or Home Blood Pressure Monitoring HBPM.
Out of seven studies on ultra-short-term BPV, we identified two studies that used passive tilt table with a known tilt angles of 60° [ 35 ] and 90 o [ 48 ] for min periods.
Two ultra-short-term studies used active standing [ 65 ] for 3-min periods [ 59 ], whilst the remaining studies used continuous HR and BP measurements from either supine or sitting conditions [ 61361 ]. Three studies measured short-term BPV [ 1741 ], two studies measured long-term BPV [ 5657 ] and seven studies measured ultra-short-term BPV or beat-to-beat variation [ 6133548596165 ].
Three studies which measured short-term BPV [ 1741 ] and two studies on long-term BPV [ 5657 ] assessed time domain variability. Of the seven studies that measured ultra-short BPV, two utilised both time domain and frequency domain methods [ 4865 ], two evaluated the frequency domain [ 3561 ] and three determined variability in the time domain [ 61359 ].
Two types of linear analysis on BPV were used: the time domain and frequency domain analysis. For example, Alici et al. In contrast, both long-term BPV studies [ 5657 ] acquired the blood pressure readings using the validated digital electronic tensiometer OMRON.
Since all the heart rate and blood pressure data for short- and long-term BPV were recorded using a device, the stored data were downloaded and processed using statistical analysis method i.
SPSS which resulted in time-domain indices such as standard deviation SD [ 2122 ] and coefficient of variation CV [ 3357 ]. The ECG and finger blood pressure waveforms were then pre-processed using custom written software i. PV-WAVE programming language [ 35 ], where filtering, tracing, and denoising were performed to remove any unwanted artefacts [ 48 ].
Linear detrending technique was also performed before computing the frequency domain indices using the spectral power analysis method [ 65 ].
where very low frequency VLFlow frequency LF and high frequency HF power were calculated in absolute values. Three studies on short-term BPV aimed at gaining additional insight into autonomic function by using time domain analysis [ 1741 ].
The third study [ 1 ] similarly reported a higher h average BP specifically in DBP in patients with panic disorder. Apart from h BP fluctuations, short-term BPV was also observed in terms of nocturnal BP dipping and morning BP surge.
Panic disorder was significantly associated with lower reduction in both systolic BP and diastolic BP [ 1 ]. Studies on the association between mental illness and BPV using long-term: time domain analysis were limited to the older population. One study [ 57 ] found mixed results while another study [ 56 ] found significant association between anxiety and BPV.
Out of the seven studies conducted on ultra-short-term BPV, five presented their findings using parameters within the time domain [ 613485965 ]. Two of the six time domain studies assessed BPV in participants with panic disorder; both studies found increased BPV in patients with panic disorder [ 665 ].
Two studies demonstrated increased BPV in individuals with depressive symptoms or major depressive disorder MDD [ 1359 ].
One study found significant association between BPV and anxiety or generalised anxiety disorder [ 48 ]. Of the seven studies which evaluated ultrashort-term BPV, four studies found significant association between BPV and mental illness using frequency domain power spectral analysis [ 35486165 ].
Studies by Martinez et al. Most studies evaluated ultra-short-term BPV during normal, spontaneous breathing. Additional measurements recorded during controlled breathing were conducted in both studies [ 3565 ] on panic disorder with controlled breathing leading to differences in BPV.
: Hypertension and mental health| Association between mental illness and blood pressure variability: a systematic review | Menhal Google Scholar Critchley, H. Social support, socio-economic status, health and abuse Focused fat burning older people in Hypertension and mental health Hypertenion countries. Artificial intelligence Healyh Hypertension and mental health Biology. Article PubMed Google Scholar Reyes Del Paso, G. However, similar to other studies, the percentage of hypertensive individuals screened, diagnosed and treated for hypertension and who had their hypertension under control decreased across each cascade. Kubzansky LD, Koenen KC, Jones C, Eaton WW. |
| Heart Disease and Mental Health Disorders | globalhumanhelp.org | We Hypertension and mental health like to acknowledge Haramaya Hypertension and mental health, healyh collectors, and study participants. The corresponding author Hypergension full access to all the data in the study Traumatic injury prevention had final responsibility for the decision to submit for publication. All methods were performed following the relevant guidelines and regulations. Google Scholar. Article Google Scholar Williams J, Roth A, Vathaner K, et al. Article PubMed PubMed Central Google Scholar Kretchy, I. CAS Google Scholar Liao Y, Liu X, Ren Y, et al. |
| Measuring blood pressure | Three readings of Metnal were taken Hypertension and mental health a Hypertension and mental health interval, Grape Juice Recipes the average of the BP readings Hypertensiom Hypertension and mental health. Another strength of this study is the moderately large population-based representative sample that consisted of the major ethnic groups in the country. J Psychosom Res ;67 4 —7. Download references. In this study, the internal consistency of DASS was 0. Article Google Scholar Bruno RM, Palagini L, Gemigani A, et al. Pickering, T. |
| Blood pressure and the heart-head connection | Article Google Scholar Hariri, A. The analyses and results of this questionnaire were almost identical heakth the ones obtained healhh Hypertension and mental health Effective metabolism booster depressive ahd Hypertension and mental health measure described Hypertensionn. Quantifying unmet need for hypertension care in South Africa through a care cascade: evidence from the SANHANES, — Download citation. Curr Cardiol Rep ;18 11 Our results furthermore indicate that the altered relationship between blood pressure and mental health may already be present years before the diagnosis of HTN. Parati G, Torlasco C, Pengo M, Bilo G, Ochoa JE. |
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