Romit Bhattacharya
@romitb.bsky.social
Preventive Cardiologist at Mass General Hospital | Lifestyle, Genomics, Digital Health, South Asian CVD
Our combined model accounted for just shy of 85% of the risk of incident MI, but factors like diet and exercise underperformed.
We wonder if healthy participant bias, or self report were to blame here?
In a cohort with more lifestyle phenotyping would this improve?
Criticism welcome
We wonder if healthy participant bias, or self report were to blame here?
In a cohort with more lifestyle phenotyping would this improve?
Criticism welcome
July 3, 2025 at 2:00 PM
Our combined model accounted for just shy of 85% of the risk of incident MI, but factors like diet and exercise underperformed.
We wonder if healthy participant bias, or self report were to blame here?
In a cohort with more lifestyle phenotyping would this improve?
Criticism welcome
We wonder if healthy participant bias, or self report were to blame here?
In a cohort with more lifestyle phenotyping would this improve?
Criticism welcome
Zooming in on the base of the graph yields further insights.
While WHR has a lower R2 - in a society where obesity is increasingly common it accounts for a greater population risk
Dyslipidemia is the opposite - greater R2, but decreasing burden
Lp(a) and hsCRP are comparable!
While WHR has a lower R2 - in a society where obesity is increasingly common it accounts for a greater population risk
Dyslipidemia is the opposite - greater R2, but decreasing burden
Lp(a) and hsCRP are comparable!
July 3, 2025 at 2:00 PM
Zooming in on the base of the graph yields further insights.
While WHR has a lower R2 - in a society where obesity is increasingly common it accounts for a greater population risk
Dyslipidemia is the opposite - greater R2, but decreasing burden
Lp(a) and hsCRP are comparable!
While WHR has a lower R2 - in a society where obesity is increasingly common it accounts for a greater population risk
Dyslipidemia is the opposite - greater R2, but decreasing burden
Lp(a) and hsCRP are comparable!
When we looked at population attributable risk, we found that PAR took the number one spot, with HTN at a close second, and comparing both R2 and PAR stand apart
Perhaps HTN is a good integrator of the risk imparted by other risk factors
Perhaps PRS is the primordial risk factor for all others
Perhaps HTN is a good integrator of the risk imparted by other risk factors
Perhaps PRS is the primordial risk factor for all others
July 3, 2025 at 2:00 PM
When we looked at population attributable risk, we found that PAR took the number one spot, with HTN at a close second, and comparing both R2 and PAR stand apart
Perhaps HTN is a good integrator of the risk imparted by other risk factors
Perhaps PRS is the primordial risk factor for all others
Perhaps HTN is a good integrator of the risk imparted by other risk factors
Perhaps PRS is the primordial risk factor for all others
We examined performance in 3 ways: by R2, C-statistic and PAR.
In our R^2 leave-one-out approach, hypertension and a polygenic risk score (GPSmult @aniruddhpatelmd.bsky.social ) that integrated CVD risk factors performed better than all other risk factors.
cc: @somijemmacho.bsky.social
In our R^2 leave-one-out approach, hypertension and a polygenic risk score (GPSmult @aniruddhpatelmd.bsky.social ) that integrated CVD risk factors performed better than all other risk factors.
cc: @somijemmacho.bsky.social
July 3, 2025 at 2:00 PM
We examined performance in 3 ways: by R2, C-statistic and PAR.
In our R^2 leave-one-out approach, hypertension and a polygenic risk score (GPSmult @aniruddhpatelmd.bsky.social ) that integrated CVD risk factors performed better than all other risk factors.
cc: @somijemmacho.bsky.social
In our R^2 leave-one-out approach, hypertension and a polygenic risk score (GPSmult @aniruddhpatelmd.bsky.social ) that integrated CVD risk factors performed better than all other risk factors.
cc: @somijemmacho.bsky.social
In the UKBB and MGBB we build a Clinical and Genetic/Biomarker model of disease.
Traditional risk factors included: HTN, ApoB:ApoA1, T2D, EtOH, WHR, TDI, exercise and Diet
Genetic/Biomarkers Added: PRS, HeFH variants, Lp(a) and hsCRP
Traditional risk factors included: HTN, ApoB:ApoA1, T2D, EtOH, WHR, TDI, exercise and Diet
Genetic/Biomarkers Added: PRS, HeFH variants, Lp(a) and hsCRP
July 3, 2025 at 2:00 PM
In the UKBB and MGBB we build a Clinical and Genetic/Biomarker model of disease.
Traditional risk factors included: HTN, ApoB:ApoA1, T2D, EtOH, WHR, TDI, exercise and Diet
Genetic/Biomarkers Added: PRS, HeFH variants, Lp(a) and hsCRP
Traditional risk factors included: HTN, ApoB:ApoA1, T2D, EtOH, WHR, TDI, exercise and Diet
Genetic/Biomarkers Added: PRS, HeFH variants, Lp(a) and hsCRP
The statistic that 80-90% of all CVD risk is due to these factors is often cited, but this is at odds with what we see in the clinic.
Many patients struggle more than others to control their risk factors - often due to polygenic risk, monogenic variants, or other risk factors.
We integrated both
Many patients struggle more than others to control their risk factors - often due to polygenic risk, monogenic variants, or other risk factors.
We integrated both
July 3, 2025 at 2:00 PM
The statistic that 80-90% of all CVD risk is due to these factors is often cited, but this is at odds with what we see in the clinic.
Many patients struggle more than others to control their risk factors - often due to polygenic risk, monogenic variants, or other risk factors.
We integrated both
Many patients struggle more than others to control their risk factors - often due to polygenic risk, monogenic variants, or other risk factors.
We integrated both
INTERHEART & the Global Risk Factors Consortium showed that modifiable risk factors account for most risk
www.nejm.org/doi/full/10....
So then how do genetic risk factors like Polygenic risk, Heterozygous FH variants, and novel biomarkers like Lp(a) [also genetic!] and hsCRP play a role?
www.nejm.org/doi/full/10....
So then how do genetic risk factors like Polygenic risk, Heterozygous FH variants, and novel biomarkers like Lp(a) [also genetic!] and hsCRP play a role?
Global Effect of Modifiable Risk Factors on Cardiovascular Disease and Mortality | NEJM
Five modifiable risk factors are associated with cardiovascular disease and death from any cause. Studies using individual-level data to evaluate the regional and sex-specific prevalence of the ris...
www.nejm.org
July 3, 2025 at 2:00 PM
INTERHEART & the Global Risk Factors Consortium showed that modifiable risk factors account for most risk
www.nejm.org/doi/full/10....
So then how do genetic risk factors like Polygenic risk, Heterozygous FH variants, and novel biomarkers like Lp(a) [also genetic!] and hsCRP play a role?
www.nejm.org/doi/full/10....
So then how do genetic risk factors like Polygenic risk, Heterozygous FH variants, and novel biomarkers like Lp(a) [also genetic!] and hsCRP play a role?
#JohnHawley tells us about Exercise Mimetics
- A compound that increased skeletal muscle gene programs, did not have any effect in performance without at least some exercise.
- he frames exercise mimetics more as augmentative therapies than therapies that replace exercise
- A compound that increased skeletal muscle gene programs, did not have any effect in performance without at least some exercise.
- he frames exercise mimetics more as augmentative therapies than therapies that replace exercise
June 4, 2025 at 3:54 PM
#JohnHawley tells us about Exercise Mimetics
- A compound that increased skeletal muscle gene programs, did not have any effect in performance without at least some exercise.
- he frames exercise mimetics more as augmentative therapies than therapies that replace exercise
- A compound that increased skeletal muscle gene programs, did not have any effect in performance without at least some exercise.
- he frames exercise mimetics more as augmentative therapies than therapies that replace exercise
Using a multi-omics approach, changes in mitochondrial associated analytes were found across tissue types (particularly at the transcriptome level)
June 4, 2025 at 3:21 PM
Using a multi-omics approach, changes in mitochondrial associated analytes were found across tissue types (particularly at the transcriptome level)
@malenelindholm.bsky.social from Stanford shares about the molecular basis of exercise adaptations!
- Describing the NIH-funded MoTrPAC study
- OMics and the mitochondrial response to exercise
- Sex differences in skeletal muscle responses!
- Describing the NIH-funded MoTrPAC study
- OMics and the mitochondrial response to exercise
- Sex differences in skeletal muscle responses!
June 4, 2025 at 2:59 PM
@malenelindholm.bsky.social from Stanford shares about the molecular basis of exercise adaptations!
- Describing the NIH-funded MoTrPAC study
- OMics and the mitochondrial response to exercise
- Sex differences in skeletal muscle responses!
- Describing the NIH-funded MoTrPAC study
- OMics and the mitochondrial response to exercise
- Sex differences in skeletal muscle responses!
& Fascinating results of exercise slowing breast cancer metastases in mice
June 4, 2025 at 2:55 PM
& Fascinating results of exercise slowing breast cancer metastases in mice
#MarkFebbraio discussing how exercise can protect against the progression of #lifestyle diseases
- Exercise protects against and reverses MASH
- Integrin beta 5 as a key regulator of muscle-liver cross-talk
- Purified EVs from exercising animals and reverse MASH
- Exercise protects against and reverses MASH
- Integrin beta 5 as a key regulator of muscle-liver cross-talk
- Purified EVs from exercising animals and reverse MASH
June 4, 2025 at 2:55 PM
#MarkFebbraio discussing how exercise can protect against the progression of #lifestyle diseases
- Exercise protects against and reverses MASH
- Integrin beta 5 as a key regulator of muscle-liver cross-talk
- Purified EVs from exercising animals and reverse MASH
- Exercise protects against and reverses MASH
- Integrin beta 5 as a key regulator of muscle-liver cross-talk
- Purified EVs from exercising animals and reverse MASH
EVs carrying an incredible diversity of proteins in the post-exercise individuals across a number of functional classes - including active kinases in particular AMPK
Transferring exercise EVs from athletic mice to sedentary mice seems to reduce fat mass and markers of fatty liver!
Transferring exercise EVs from athletic mice to sedentary mice seems to reduce fat mass and markers of fatty liver!
June 4, 2025 at 2:07 PM
EVs carrying an incredible diversity of proteins in the post-exercise individuals across a number of functional classes - including active kinases in particular AMPK
Transferring exercise EVs from athletic mice to sedentary mice seems to reduce fat mass and markers of fatty liver!
Transferring exercise EVs from athletic mice to sedentary mice seems to reduce fat mass and markers of fatty liver!
#MartinWhithamPhD from Birmingham tells us about techniques to decode exercise-responsive signaling networks, particularly those mediated by extracellular vesicles!
Can EVs from exercising subjects confer benefits to sedentary individuals?
Can EVs from exercising subjects confer benefits to sedentary individuals?
June 4, 2025 at 2:07 PM
#MartinWhithamPhD from Birmingham tells us about techniques to decode exercise-responsive signaling networks, particularly those mediated by extracellular vesicles!
Can EVs from exercising subjects confer benefits to sedentary individuals?
Can EVs from exercising subjects confer benefits to sedentary individuals?
While weight loss alone does not correct both of these deficits, but weight loss WITH exercise improves both!
June 4, 2025 at 1:39 PM
While weight loss alone does not correct both of these deficits, but weight loss WITH exercise improves both!
Lean subjects utilize fatty acid metabolism during a fast and quickly switch to carbohydrate metabolism with insulin.
Whereas, insulin-resistant pts were inefficient oxidizers of fatty acids during fasting, and were less efficient in switching to carbohydrate metabolism when exposed to insulin.
Whereas, insulin-resistant pts were inefficient oxidizers of fatty acids during fasting, and were less efficient in switching to carbohydrate metabolism when exposed to insulin.
June 4, 2025 at 1:30 PM
Lean subjects utilize fatty acid metabolism during a fast and quickly switch to carbohydrate metabolism with insulin.
Whereas, insulin-resistant pts were inefficient oxidizers of fatty acids during fasting, and were less efficient in switching to carbohydrate metabolism when exposed to insulin.
Whereas, insulin-resistant pts were inefficient oxidizers of fatty acids during fasting, and were less efficient in switching to carbohydrate metabolism when exposed to insulin.
#BretGoodPasterPhD speaks to us about intramyocellular lipids and insulin resistance and a VERY fascinating concept of metabolic flexibility:
June 4, 2025 at 1:30 PM
#BretGoodPasterPhD speaks to us about intramyocellular lipids and insulin resistance and a VERY fascinating concept of metabolic flexibility:
#MichaelSnyder from #StanfordGenetics gives the Blackburn Keynote and covers:
- Ageotypes (people age in different patterns, in different organs)
- 2 major aging timepoints at age 44 and 60
- The post-exercise compound Lac-Phe regulate appetite and obesity
- Using Wearables for lifestyle monitoring
- Ageotypes (people age in different patterns, in different organs)
- 2 major aging timepoints at age 44 and 60
- The post-exercise compound Lac-Phe regulate appetite and obesity
- Using Wearables for lifestyle monitoring
June 4, 2025 at 12:59 PM
#MichaelSnyder from #StanfordGenetics gives the Blackburn Keynote and covers:
- Ageotypes (people age in different patterns, in different organs)
- 2 major aging timepoints at age 44 and 60
- The post-exercise compound Lac-Phe regulate appetite and obesity
- Using Wearables for lifestyle monitoring
- Ageotypes (people age in different patterns, in different organs)
- 2 major aging timepoints at age 44 and 60
- The post-exercise compound Lac-Phe regulate appetite and obesity
- Using Wearables for lifestyle monitoring
