實證營養報告

1. 實證營養報告 張秋密0824

2. Clinical Scenario臨床劇本 請問喝飲料可能會增加尿酸嗎？ Since the introduction into the US food supply in the 1970s, high fructose corn syrup has become the most popular sweetener used in processed foods, especially in beverages such as sodas and fruit drinks. Fructose, unlike glucose or other monosaccharide sugars, is solely metabolized in the liver where it induces nucleotidecatabolism, thereby producing uric acid. Human studies confirm that experimental fructose feeding or intravenous fructose administration raises serum uric acid levels. This may be important because serum uric acid has been suggested to be a marker of cardiovascular disease risk and a potential intermediate step towards the development of hypertension.

3. Step 1: Ask an answerable clinical question--P.I.C.O.形成一個可以回覆的問題

4. PICO Question: Patient / Problem : adolescent青春期的人 Intervention / Exposure : sugar sweetened beverage consumption喝含糖飲料量 Comparison : none 無 Outcome : 尿酸值增高(Aetiology 病因學) Ex: whether the consumption of sugar sweetened beverages is associated with higher serum uric acid levels, and with higher blood pressure, in a representative sample of adolescents.（在青春期的族群中，喝飲料是否增高尿酸？）

5. Step 2: Effective searches for the best Evidence搜尋最佳的證據

6. 搜尋策略的設計表 SEARCH STRATEGY DESIGN TABLE

10. Etiology (病因) • 橫斷性研究（Cross-sectional study）: 在某一時間點進行的研究 • Study Populations • There were 4938 adolescents aged 12 to18 years with dietary intake data and serum uric acid levels measured in National Health and Nutrition Examination Survey (NHANES) 1999–2004. We excluded pregnant adolescents (n= 71). Thus,there were 4867 adolescents available for this analysis. • Dietary data was assessed from 24-hour dietary recall interviews. • Sugar sweetened beverages included fruit drinks, sports drinks,soda, and sweetened coffee or tea. • We used multivariate linear regression to evaluate the association of sugar sweetened beverage consumption with serum uric acid and with blood pressure.

11. Step 3: Critically appraise that evidence for its validity and importance嚴格評讀文獻是否令人信服及其重要性

12. A.此一有害原因的研究結果能令人信服嗎?Are the results of this harm/etiology study valid?

13. 1.實驗組與對照組除了對治療的曝露有別外, 其他方面是否皆相似? Were there clearly defined groups of patients, similar in all important ways other than exposure to the treatment or other cause? No table 1

14. Interaction terms with P < 0.20 were designated à priori as significant.

15. 2.實驗組與對照組的評量方法是否相同? Were treatments/ exposures and clinical outcomes measured in the same ways in both groups (Was the assessment of outcomes either objective or blinded to exposure?) Yes 各組皆依照喝飲料量分析受測者尿酸及血壓的變化情形。

16. 3.追蹤夠久、夠完整嗎? Was the follow-up of the study patients sufficiently long (for the outcome to occur) and complete? Yes

17. 4.因果關係夠明確嗎?Do the results of the harm study satisfy some of the diagnostic tests for causation? a.曝露在發作之前嗎? Is it clear that the exposure preceded the onset of the outcome? b.與劑量具有相關反應嗎? Is there a dose-response gradient? c.從”去曝露--再曝露”的研究上有正面證據嗎? Is there any positive evidence from a “dechallenge-rechallenge” study? d.因果關係具有生物學上的意義嗎? Does the association make biological sense? a. unclear.This article didn’t mention about it. b.Yes，由table 2及table 3可以得知：飲料喝愈多，尿酸及收縮壓愈高，且有顯著差異 NO Yes

18. 1999–2004 We found that the correlation of sugar sweetened beverage consumption with serum uric acid levels was not modified by sex or obesity (P for interaction > 0.2 each). The observed serum uric acid difference between extreme categories, 0.18mg/dL, in the NHANES III, was associated with an 50% increased risk of incident gout in a large prospective adult cohort study.11, 24 On the other hand, for every 1mg/dL increase in serumuric acid, there was a 7% increase in the development of incident kidney disease or death afteradjusting for multiple variables such as age, sex, race, systolic blood pressure, alcohol,smoking, HDL-cholesterol, and baseline kidney

19. 2.暴露與結果之相關性的估計有多精準？What is the precision of the estimate of the association between the exposure and the outcome? Figure 1. Sample mean of serum uric acid with 95% confidence intervals by categories of sugar sweetened beverage consumption adjusted for age, race/ethnicity, sex, total calories, BMI zscore, alcohol, smoking, dietary fiber intake, diet beverage consumption, and milk consumption. P for trend = 0.01

20. We found that the correlation of sugar sweetened beverage consumption with blood pressure was not modified by sex or obesity (P for interaction > 0.2 each). The mean systolic blood pressure z-score increased by 0.17 for the highest sugar sweetened beverage category. This represents a difference of 2mmHg (95% CI 1–2mmHg). In a general normotensive adult population, a 2mmHg reduction of systolic blood pressure would lower stroke mortality by 10% and ischemic heart disease by 7%.26

21. B.此一有害原因的研究結果夠重要嗎? Are the valid results of this harm study important?

22. 1.暴露與結果之間的相關性有多強？What is the magnitude of the association between the exposure and outcome? (OR) = ad/bc NNH=1/[a/(a+b)−c/(c+d)] ※研究結果無發生痛風及高血壓的個案數，所以無法計算OR、NNH，只能看相對風險(RR)的部分

23. 飲料量對於尿酸及血壓值的影響 • 飲料喝愈多，尿酸及收縮壓愈高，且有顯著差異

24. C.此一令人信服且結果重要的研究的會改變我們對病患的治療嗎?C.此一令人信服且結果重要的研究的會改變我們對病患的治療嗎? Can this valid and important evidence about harm be applied to our patient?

25. 1.我們的病患與研究中收錄的病患有明顯不同，以致於無法應用該研究的結果？Is our patient so different from those included in the study that its results cannot apply? • No • 研究對象與平常我們接觸的病人條件類似 2.此項治療對我們的病患潛在的益處為何?潛在的危害為何?What is our patient’s risk of benefit and harm from the agent? • 由本研究可以得知：飲料喝愈多，尿酸及收縮壓愈高，且有顯著差異 • 這可以告訴病人應該要注意飲料量，以避免日後尿酸及血壓增高，增加痛風及高血壓發生的危險性。

26. 3.我們的病人對治療的偏好、關心與期待為何?What are our patient’s preferences, concerns, and expectations from this treatment? • 希望飲料喝愈少愈好 4.有哪些替代治療?What alternative treatments are available? • 建議病人多喝白開水、 飲料稀釋、 飲食清淡、避免菸酒，相信痛風及高血壓發生的機會能減至最低。

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