18 research outputs found

    Mortality by Weight Change in 1975–1981 among Those with No Intention to Lose Weight in 1975

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    <p>Probability of survival from baseline in 1982 through 1999 among 1,899 participants who in 1975 reported no intention to lose weight and who either lost weight, gained more than 1.0 kg/m<sup>2</sup> in BMI, or remained stable, i.e., were unchanged or gained less than 1.0 kg/m<sup>2</sup> in BMI, between 1975 and 1981. The survival probability was adjusted as in <a href="http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0020171#pmed-0020171-g001" target="_blank">Figure 2</a>. Note that the participants with weight loss had about the same survival rates throughout the 18 y of observation as those with stable weight, whereas those gaining weight showed a lower survival rate.</p

    Mortality by Weight Change in 1975–1981 among Those Reporting Trying to Lose Weight in 1975

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    <div><p>Probability of survival from baseline in 1982 through 1999 among 1,058 participants who in 1975 reported intention to lose weight and who either lost weight, gained more than 1.0 kg/m<sup>2</sup> in BMI, or remained stable, i.e., were unchanged or gained less than 1.0 kg/m<sup>2</sup> in BMI, between 1975 and 1981.</p> <p>The survival probability was adjusted using the Cox regression model for sex, median age, and median BMI. Note that the participants with weight loss had a lower survival rate throughout the 18 y of observation, whereas those with stable weight and weight gain did not differ.</p></div

    Flowchart Shows the Delineation of the Study Sample by Various Exclusions

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    <p>MI, myocardial infarction; COPD, chronic obstructive pulmonary disease</p

    Flow chart of the data collection of eating disorder study in males of FinnTwin16 cohorts.

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    <p>* Excluded N = 10 men whose low BMI resulted from missing limbs or tetraplegia; or other severe physical illness (multiple sclerosis, cerebral palsy).</p

    Figure 8

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    <p>Correlations with classical lipid parameters using Spearman rank correlations across all individuals (<i>N</i> = 48). Only lipids with <i>p</i><0.1 are reported for triglyceride and total cholesterol correlations. <sup>*</sup><i>p</i><0.05, <sup>**</sup><i>p</i><0.01, ***<i>p</i><0.001.</p

    Figure 9

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    <p>Correlation of serum triglyceride measure with different triacylglycerol species as a function of (A) the amount, and (B) the number of fatty acid carbons.</p

    Figure 4

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    <p>Twin-normalized Spearman rank correlations of (A) two most abundant lysophosphatidylcholine and (B) ether phospholipid species with clinical variables. <sup>*</sup><i>p</i><0.05, <sup>**</sup><i>p</i><0.01.</p

    Figure 5

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    <p>Correlation plots for selected sphingomyelin species and clinical variables in (A) individual twins, and (B) twin pairs.</p

    Figure 3

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    <p>Partial least squares discriminant analysis (PLS/DA) of lipidomics profiles for obesity discordant co-twins, utilizing only the 133 identified peaks and two classes (obese and non-obese co-twins) to build the model. Three latent variables were used (Q<sup>2</sup> = 47%). (A) PLS/DA score plot. Genders and twin-pair identifiers are marked for each sample, although this information was not used to build the model. (B) Fold changes for most important variables based on VIP analysis contributing to the PLS/DA model.</p
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