## 3 Results
### Genetic Profile  
A genetic analysis was conducted to evaluate participants' predisposition to metabolic alterations, inflammatory status, neuromuscular regulation, and nutrient intolerance. The objective was to assess the distribution of key genetic variants and explore whether baseline genetic predispositions could modulate the physiological response to algae-based supplementation.  
The analysis included variants related to anxiety, dopamine regulation, appetite control, sugar addiction, systemic inflammation, insulin resistance, metabolic syndrome, and intolerances to gluten, lactose, and fructose. Additionally, predisposition to vitamin D and B12 deficiencies and blood clotting risk were assessed.  
Table 2 shows the absolute and relative frequency distributions of genetic profiles across both groups. A chi-square test was used to evaluate between-group differences in genotype frequencies. No statistically significant differences were observed between the intervention and control groups for any of the polymorphisms analyzed (\(p>0.05\)), suggesting that the groups were genetically comparable at baseline. This supports the internal validity of the trial by minimizing the likelihood that genetic variation confounded the observed intervention effects.  
\begin{table}
\begin{tabular}{c c c c} \hline \hline
**Variable** & **Category** & \
\begin{tabular}{c} **Algae Supplement** \\ **Group, n (\%)** \\ \end{tabular} &
\begin{tabular}{c} **Control Group, n** \\ **(\%)** \\ \end{tabular} \\ \hline \multirow{4}{*}{Anxiety} & Low & 13 (18.6\%) & 12 (17.1\%) \\ \cline{2-4}  & Average & 8 (11.4\%) & 7 (10.0\%) \\ \cline{2-4}  & Protected & 14 (20.0\%) & 16 (22.9\%) \\ \hline \multirow{4}{*}{Dopamine} & Low & 11 (15.7\%) & 13 (18.6\%) \\ \cline{2-4}  & Average & 8 (11.4\%) & 8 (11.4\%) \\ \cline{2-4}  & Protected & 16 (22.9\%) & 14 (20.0\%) \\ \hline \multirow{4}{*}{Appetite} & Low & 7 (10.0\%) & 9 (12.9\%) \\ \cline{2-4}  & Average & 17 (24.3\%) & 17 (24.3\%) \\ \cline{2-4}  & Protected & 11 (15.7\%) & 9 (12.9\%) \\ \hline \multirow{4}{*}{Sugar Addiction Predisposition} & Low & 9 (12.9\%) & 10 (14.3\%) \\ \cline{2-4}  & Average & 11 (15.7\%) & 13 (18.6\%) \\ \cline{2-4}  & Protected & 15 (21.4\%) & 12 (17.1\%) \\ \hline \multirow{4}{*}{Inflammation Predisposition} & Low & 10 (14.3\%) & 8 (11.4\%) \\ \cline{2-4}  & Low / Average & 9 (12.9\%) & 9 (12.9\%) \\ \cline{2-4}  & Average & 16 (22.9\%) & 18 (25.7\%) \\ \hline \multirow{2}{*}{Insulin Resistance} & Average & 19 (27.1\%) & 18 (25.7\%) \\ \cline{2-4}  & Protected & 16 (22.9\%) & 17 (24.3\%) \\ \hline \multirow{4}{*}{Metabolic Syndrome} & Average & 22 (31.4\%) & 20 (28.6\%) \\ \cline{2-4}  & At risk & 7 (10.0\%) & 9 (12.9\%) \\ \cline{2-4}  & Protected & 6 (8.6\%) & 6 (8.6\%) \\ \hline \multirow{4}{*}{Gluten Intolerance} & At risk for celiac disease & 16 (22.9\%) & 16 (22.9\%) \\ \cline{2-4}  & No risk haplotypes & 19 (27.1\%) & 19 (27.1\%) \\ \hline \hline \end{tabular}
\end{table}
Table 2: Distribution of gene frequencies.  
To assess the potential influence of genetic predisposition on the variability of metabolic, oxidative, and inflammatory markers, a series of one-way ANOVA tests were conducted using each genetic variable as a grouping factor. No statistically significant associations (\(p>0.05\)) were found between any of the genetic categories and the baseline levels of biochemical markers such as HbA1c, lipid profile (HDL, LDL, triglycerides), malondialdehyde, catalase, myeloperoxidase, or erythrocyte sedimentation rate. However, a trend toward significance was observed for cortisol levels in relation to genetic predisposition to insulin resistance (F = 3.97, \(p=0.050\)), suggesting a potential influence of this genotype on stress-related hormonal regulation. While this finding did not reach the conventional threshold for statistical significance, it may warrant further investigation in future studies with larger samples.