Results

Question 1

Primary protective finding for hPDI in prediabetes?

Answer 1

Each ↑ tertile of hPDI linked to 12 % ↓ CVD risk (HR 0.88, 95 % CI 0.79–0.98; p = 0.025).

Question 2

Was the same hPDI benefit seen in diabetes?

Answer 2

No significant effect (HR 1.00, 95 % CI 0.89–1.14; p = 0.97).

Question 3

Key detrimental finding for uPDI in prediabetes?

Answer 3

Highest vs lowest tertile gave 17 % ↑ CVD risk (HR 1.17, 95 % CI 1.05–1.30; p = 0.005).

Question 4

uPDI effect size in diabetes?

Answer 4

14 % higher CVD risk (HR 1.14, 95 % CI 1.00–1.29; p = 0.043).

Question 5

Overall PDI association with CVD (both groups)?

Answer 5

Null – no significant link in prediabetes (HR 1.05) or diabetes (HR 0.96).

Question 6

Which CVD subtype rose with uPDI in prediabetes?

Answer 6

Coronary heart disease (CHD) ↑ 17 % (HR 1.17; p = 0.038).

Question 7

Any stroke signal in main models?

Answer 7

Stroke ↑ with uPDI in age/sex model, but association attenuated after full adjustment.

Question 8

% of hPDI-CVD relation explained by SSB intake?

Answer 8

35 % mediation (p = 0.005).

Question 9

% of uPDI-CVD relation in diabetes explained by low whole-grain intake?

Answer 9

36 % (p = 0.028).

Question 10

Top serum biomarker mediator for uPDI → CVD?

Answer 10

Cystatin C (15 % of effect in prediabetes; 44 % in diabetes; p < 0.001).

Question 11

IGF-1 role in T2D subgroup?

Answer 11

Mediated 37 % of hPDI-CVD pathway (p = 0.049).

Question 12

Whole-grain vs CVD in diabetes – direction?

Answer 12

Higher whole-grain intake ↓ CVD risk; deficit drives 36 % of uPDI harm.

Question 13

SSBs – harm or help?

Answer 13

Harm : high SSBs account for 15 % of uPDI-CVD risk.

Question 14

Subgroup where hPDI benefit was strongest?

Answer 14

Participants < 60 y, non-smokers, no family history of diabetes.

Question 15

Subgroup most vulnerable to uPDI harm?

Answer 15

Low Townsend Deprivation Index (TDI) & non-vitamin users.

Question 16

Interpretation when HR < 1?

Answer 16

Protective (lower hazard vs reference).

Question 17

Interpretation when HR > 1?

Answer 17

Increased risk relative to reference group.

Question 18

Median follow-up time contributing to results?

Answer 18

~ 9.6 years (diabetes) / 9.9 years (prediabetes).

Question 19

Total CVD events captured (prediabetes)?

Answer 19

2 324 events over 172 610 person-years.

Question 20

Total CVD events captured (diabetes)?

Answer 20

1 461 events over 74 951 person-years.

Question 21

Model 2 adjusted for which broad covariate categories?

Answer 21

Socio-demographics, lifestyle, clinical history, & (in diabetes) duration of disease.

Question 22

Why were events within 2 y of baseline excluded in sensitivity tests?

Answer 22

To reduce reverse causality (diet change due to subclinical disease).

Question 23

Did sensitivity analyses change core findings?

Answer 23

No – uPDI remained harmful; hPDI protective only in prediabetes.

Question 24

Key takeaway in one sentence?

Answer 24

Diet quality matters: unhealthy plant-based eating ↑ CVD risk, while healthful patterns confer modest protection in prediabetes.

Question 25

Clinically, what diet mod to prioritise from mechanisms data?

Answer 25

Boost whole-grains & cut SSBs/animal fat to shift uPDI → hPDI.

Question 26

Mechanistic biomarker suggesting kidney-cardio link?

Answer 26

Cystatin C (renal dysfunction marker) mediates large share of risk.

Question 27

What does a 36 % ‘explained effect’ mean?

Answer 27

Whole-grains account for 36 % of the total uPDI → CVD association in diabetes—implying partial causality.

Question 28

Why no blanket benefit of plant-based quantity (PDI)?

Answer 28

Without quality filters, plant foods can be refined/ultra-processed, diluting cardio-protection.

Question 29

Stat test used for main hazard ratios?

Answer 29

Cox proportional-hazards models.

Question 30

Lightning-round mantra?

Answer 30

“hPDI helps pre-diabetics, uPDI hurts everyone.”