Indian Barberry and Milk Thistle for Blood Glucose Metabolism and Liver Function Support

Herbs and Nutrients That May Assist

Chromium picolinate
Chromic chloride hexahydrate
Berberine hydrochloride derived from Indian barberry
Berberis aristate, root
Milk thistle
Silybum marianum, seed

Actions

  • Reduces the metabolic impacts of visceral fat
  • Preserves pancreatic beta islet cell function
  • Supports healthy blood glucose levels
  • Stimulates muscle and adipose metabolism

Clinical Applications

  • Type 2 diabetes mellitus (T2DM)
  • Polycystic ovarian syndrome (PCOS)

Clinical Overview

Clinical Overview Background Information Actions Clinical Applications Safety Information Footnotes References

Clinical Overview

Metabolic dysfunction is an emerging chronic health issue, impacting up to a quarter of the Asia-pacific region. [1] Underpinning its pathology are the impacts of fat accumulation within metabolic organs (e.g., the liver and pancreas), which promotes hepatic insulin resistance, increased glucose production, hyperinsulinaemia and eventually pancreatic beta islet cell (β-cell) failure. [2] Addressing these factors, berberine hydrochloride – a constituent within Berberis aristate (Indian barberry) has been observed in vivo to reduce visceral fat, [3],[4],[5] thereby lowering inflammation [6] and oxidative stress [7] that fuels chronic metabolic dysfunction. [8] These mechanisms are linked to improving glucose control and blood lipid profiles in humans, particularly in combination with Silybum marianum (milk thistle). [9] Additionally, chromium has been shown to support metabolic balance. [10] Therefore, a blend of berberine hydrochloride, milk thistle and chromium can help support and preserve healthy metabolic function.

Background Information

Addressing the true cause of metabolic dysfunction

Metabolic syndrome features physiological patterns of raised insulin levels with abnormal glucose and lipid metabolism. [11] Disturbingly, these patterns are often chronic in nature, and can increase the incidence of cognitive impairment, cardiovascular disease, liver disease and reproductive disorders. [12],[13],[14] In individuals with abnormal metabolic pathology, a state of ‘energy overload’ within the liver and pancreas has been observed. [15],[16],[17] This occurs when energy intake exceeds energy storage capacity [*], resulting in visceral fat accumulation. [18] Contributing to a cluster of processes that drive metabolic imbalance, researchers describe these phenomena as the ‘twin cycle’ model. [19],[20],[21], [22] This model illustrates how visceral fat increases glucose synthesis, which is followed by insulin output. In excess, hyperinsulinaemic states stimulate triglyceride overproduction in the liver. Consequently, these dysfunctional metabolic patterns ultimately perpetuate an uncontrolled feedback loop of chronic metabolic imbalance (Figure 1). [23]

Figure 1: The twin cycle – energy unable to be stored as glycogen in muscle is converted into triglycerides via lipogenesis. In response to caloric excess, increased hepatic fat accumulation results in an overflow of lipoprotein-bound triglycerides into the pancreas, which can limit insulin output. [24]

Key: VLDL: Very-low-density lipoprotein.

Left unaddressed, visceral fat leads to organ damage

Accumulated visceral fat causes tissue damage following an oversupply of fatty acids within cells. [25],[26] This upregulates mitochondrial energy synthesis and reactive oxygen species (ROS) [†] output in response to increased fatty acid oxidation. [27] Within the liver and pancreas, high ROS activate cellular endoplasmic reticulum (ER) [‡] stress pathways [28] which stimulate pro-inflammatory mediators that promote hepatic and pancreatic damage. [29],[30],[31] Moreover, ER stress increases the activity of lipogenic liver enzymes, [32] which upregulate triglyceride synthesis, leading to greater visceral fat. [33] In light of this, botanical extracts show promise as a therapeutic solution to help break this self-perpetuating cycle. Namely, berberine and milk thistle have been demonstrated to effectively mitigate this sequence of pathological events. [34],[35],[36],[37]

Enhancing berberine absorption: Silymarin modulates P-glycoprotein pumps

Despite its therapeutic potential for metabolic dysfunction, [38],[39],[40],[41] berberine demonstrates poor oral bioavailability. [42] This appears to be due to intestinal P-glycoprotein (P-gp) mediated gut extrusion processes, which can reduce berberine absorption by up to 90%. [43] The P-gp inhibitor silymarin, a flavolignan derived from Silybum marianum, can effectively increase berberine uptake (Figure 2). [44] As such, the combination of berberine and milk thistle with standardised levels of flavolignans enhances berberine’s therapeutic bioavailability and clinical effect. [45]

Figure 2: Silymarin inhibits intestinal P-glycoprotein efflux pumps to enhance berberine uptake. [46]

Actions

Reduces the metabolic impacts of visceral fat

In animals, berberine reduces accumulated liver fat and lowers free fatty acid output in response to excess energy intake. [47],[48],[49],[50] In states of energy overload, berberine minimises mitochondrial ROS production, [51] as well as inflammatory markers in the liver, including interleukin 1-beta (IL-1β), IL-6 and tumour necrosis factor alpha (TNF-α). [52],[53],[54] Additionally, berberine enhances intracellular resilience to ROS [55] and decreases ER stress, [56] thereby limiting the activation of genes [57],[58] and enzymes [59] that upregulate lipogenesis in metabolic dysfunction.

These effects are partly linked to the inhibition of bile salt hydrolase enzymes produced by intestinal microbiota which facilitate the breakdown of taurine-conjugated bile acids (TCA). [60] Increased TCA levels have been shown to stimulate intestinal farnesoid X receptors, leading to lower expression of genes [61] and proteins [62] that promote fatty acid accumulation in the liver. [63] Berberine also induces cytochrome 7A1, [64] an enzyme that converts cholesterol into bile acids, which further promotes intestinal lipid excretion to help rebalance metabolic overload. [65]

Preserves pancreatic β-cell function

Berberine has been shown to protect pancreatic β-cell function in diabetic rodents. By reversing degenerative cell damage within islet mitochondria and ER structures, berberine can enhance insulin synthesis and secretion. [66] This was linked to offsetting ROS caused by the oxidation of surplus intracellular fat, which drives pancreatic damage. Moreover, studies indicate berberine can increase levels of regulatory sirtuin1 (SIRT1), [67] an endogenous enzyme that mitigates ER stress [68] to protect β-cell function and insulin output. [69],[70] Collectively, this evidence validates the use of berberine to help mitigate pancreatic damage. [71]

Supports healthy blood glucose levels

Berberine has been shown to enhance insulin secretion exclusively in hyperglycaemic states. [72] This indicates its ability to help balance blood sugar with a low risk of triggering hypoglycaemia when combined with other treatments. [73] Unique in its action, berberine blocks outgoing potassium elimination channels within pancreatic β-cells, which leads to an influx of intracellular calcium that stimulates greater insulin secretion. [74] Therefore, berberine can effectively protect β-cells while also increasing functional insulin output to manage elevated glucose.

Equally, chromium also supports healthy blood glucose control. [75] Low chromium levels have been noted in over 50% of individuals with type 2 diabetes mellitus (T2DM), [76] while its supplementation in these populations leads to improvements in markers of insulin resistance and hyperglycaemia. [77] Mechanistically, chromium is a nutritional cofactor for insulin signalling molecule, chromodulin, that promotes insulin-cell communication and glucose uptake. [78] As such, chromium supports insulin function, which enhances the clearance of excess glucose from the blood stream.

Stimulates muscle and adipose metabolism

In response to surplus energy stores, berberine enhances metabolism, shown to reduce total cholesterol (TC) and triglycerides (TGs), as well as lowering fasting glucose and elevated insulin in vivo. [79] Further, berberine was shown to increase high-density lipoprotein (HDL) and decrease low-density lipoprotein (LDL) [§]. [80] These effects highlight berberine’s positive impact on metabolism throughout the body - particularly within muscle [81] and adipose tissue. [82]

Shown to increase mitochondrial biosynthesis in skeletal muscle in vivo [**], berberine improves metabolic capacity of muscular tissue, which enhances the uptake of lipids and glucose. [83] This in turn helps stimulate the catabolism of excess energy substrates and improves insulin sensitivity. [84] Additionally, berberine increases mitochondrial density in mature adipose tissue in animals, which enhanced energy metabolism while offsetting weight gain following a high-fat diet. [85] As such, by upregulating the utilisation of energy within muscle and fat, berberine can help to alleviate metabolic overload and improve insulin sensitivity.

Clinical Applications


Type 2 diabetes mellitus (T2DM)

The combination of berberine and silymarin over six to twelve months was shown to lower TC, LDL and elevated TGs, while also improving HDL levels in patients with T2DM. [86],[87] Interestingly, berberine and silymarin also led to greater improvements in blood lipids when compared to metformin treatment. [88] In addition, improvement in fasting glucose, post prandial glucose, glycated haemoglobin, fasting insulin and insulin resistance were also reported, comparable to 1,500 mg/d of metformin. [89] The herbal combination has been safely used alongside a number of metabolic medications (Table 2). Moreover, in a study comparing berberine and silymarin to a placebo alongside a weight loss protocol in T2DM patients, active treatment led to a 21.6% greater decline in visceral fat. [90] Further, chromium has been found to enhance glucose control and support healthy weight management in T2DM, [91],[92] reinforcing the therapeutic value of berberine, silymarin and chromium in metabolic dysfunction. For more clinical results showcasing this combination in T2DM, refer to Table 1.


Polycystic ovarian syndrome (PCOS)

PCOS is recognised as a metabolic condition, as well as a reproductive disorder. [93] In a study conducted in 50 patients (average body mass index [BMI] >31), the combination of berberine and silymarin improved insulin sensitivity, serum lipids and hyperandrogenism (p<0.01). [94] Likewise, in 64 PCOS patients, 200 μg/d of chromium picolinate over 8 weeks reduced elevated plasma insulin levels by 22.5%, insulin resistance by 25% and TC levels by 6.2% (p<0.05). [95] Interestingly, in a study of 92 PCOS women, 200 μg/d of chromium picolinate after 12 weeks achieved comparable effects to metformin in supporting pregnancy rates, in addition to other positive effects outlined in Table 1. [96] As such, ingredients in Indian Barberry and Milk Thistle for Blood Glucose Metabolism and Liver Function Support can help lower blood lipids and elevated blood glucose in patients with metabolic dysfunction, including T2DM and PCOS.


Table 1: Summary of human clinical data that supports the use of ingredients in Indian Barberry and Milk Thistle for Blood Glucose Metabolism and Liver Function Support.

POPULATION

INTERVENTION

OUTCOME

Berberine and silymarin combination

136 obese patients with T2DM (mean age 55.5, average body mass index [BMI]>34). [97]

1,000 mg/d berberine + 210 mg/d silymarin vs. placebo in conjunction with a 20%-25% caloric deficit diet + 30 minutes exercise daily.

52 weeks; double-blind randomised, placebo-controlled trial (RCT).

Compared to placebo, berberine and silymarin treatment achieved greater effects on (p<0.05): ­­

- HOMA IR: -40% (-1.9 from 4.7) vs. -6.5% (-0.3 from 4.6).

- HbA1c: -19% (-1.5% from 7.9%) vs. -5.1% (-0.4% from 7.8%).

- Total cholesterol: -25% (-1.5 from 6.1 mmol/L) vs. -15% (-0.9 from 6.02 mmol/L).

- LDL: -33% (-1.3 from 3.9 mmol/L) vs. -22.2% (-0.87 from 3.9 mmol/L).

- HDL: +17% (+0.18 from 1.06 mmol/L) vs. +1.9% (+0.02 from 1.06 mmol/L)

- Triglycerides: -25% (-0.56 from 2.23 mmol/L) vs. -7.1% (-0.16 from 2.25 mmol/L).

- BMI: -5% greater decrease compared to placebo (-12.3% - [-4.2] vs. -7.35% [-2.5]).

- Visceral fat: -21.6% larger decline (-39% - vs. -17.4%).

- Waist circumference: -15 cm vs. --6 cm.

- Total body fat: -7% bigger decline (-8% vs. -1%).

­­22 type 2 diabetics (mean age 60, average BMI>34). [98]

1,000 mg/d berberine + 210 mg/d silymarin as add-on therapy to medication (e.g., metformin).

90 days; uncontrolled open-label pilot study.

Adjunct berberine and silymarin treatment reduced elevated metabolic markers (p<0.05):

- HOMA-IR: -26.1% (-1.8 from 6.9).

- HbA1c: -10.6% (-0.85% from 8.0%), maintained after 6 months post-treatment.

- Total cholesterol: -21% (-1.03 from 4.9 mmol/L).

- LDL: -19.2% (-0.5 from 2.7 mmol/L).

- Triglycerides: -44.4% (-0.84 from 1.9 mmol/L).

69 type 2 diabetics (mean age 67.1, BMI>25). [99]

1,000 mg/d berberine + 210 mg/d silymarin vs. 1,000 mg/d berberine alongside antidiabetic/ cholesterol lowering medication, low caloric diet and exercise prescription.

120 days; single-blind RCT.

Berberine and silymarin had greater effect than berberine alone on reducing:

- HbA1c: 1.72 x more effective vs. berberine (-12.3% [-0.99% from 8.02%] vs. -7.1% [-0.56% from 7.81%]; p<0.05).

- LDL levels: -16.9% (-0.41 from 2.4 mmol/L; p<0.004), vs. -12.1% (-0.3 from 2.5 mmol/L; p value=NS).

Both treatments shared similar effects on (p<0.007):

- FPG: -18.1% and -19% (-1.5 and -1.6 mmol/L from 8.8 and 8.7 mmol/L).

- Total cholesterol: -11.05% and -11.9% (-0.5 and -0.55 mmol/L from 4.6 and 4.65 mmol/L).

- Triglycerides: -22.6% and -21.6% (-0.39 and -0.37 mmol/L from 1.75-1.78 mmol/L).

109 T2DM adults with average BMI>25 and HbA1c >6.5% and <8.5%. [100]

HbA1c <7.5%: 1,000 mg/d berberine + 210 mg/d silymarin

HbA1c >7.5%: 1,500 mg/d berberine + 324 mg/d silymarin

vs. 1,500 mg/d metformin;

All groups: 600-kcal caloric deficit diet + physical activity.

6 months; double-blind RCT.

At six months berberine and silymarin achieved similar outcomes to metformin treatment compared to baseline (p<0.05):

- HOMA IR: -25.4% reduction (-1.3 from 5.1) vs. -27% (-1.4 from 5.2).

- HbA1c: -6.5% decrease (-0.5% from 7.6%) vs. -8% (-0.6% from 7.5%).

- Fasting insulin: -22.3% decline (-3.3 from 14.8 μIU/mL) vs. -21.7% (-3.3 from 15.2 μIU/mL).

- FPG: -6.4% decrease (-0.5 from 7.8 mmol/L) vs. -6.6% (-0.5 from 7.6 mmol/L).

- PPG: -8.2% reduction (-0.7 from 8.5 mmol/L) vs. -10.5% (-0.9 from 8.6 mmol/L).

Berberine and silymarin achieved greater improvements on plasma lipids vs. metformin (p<0.05):

- Total cholesterol: -17.8% reduction (-0.91 from 5.1 mmol/L) vs. -7.4% (-0.38 from 5.1 mmol/L).

- LDL: -26.6% decrease (-0.85 from 3.19 mmol/L) vs. -10.7% (-0.34 from 3.17 mmol/L).

- Triglycerides: -12.2% reduction (-0.21 from 1.72 mmol/L) vs. -6.43% (-0.11 from 1.79 mmol/L).­

85 type 1 diabetics (mean age 30.25, average

BMI 22.6). [101]


1,000 mg/d berberine + 210 mg/d silymarin + insulin vs. placebo + insulin.

6 months; double-blind RCT.

Berberine and silymarin improved insulin sensitivity compared to placebo(p<0.05):

- HbA1c: -5% decrease (-0.4% from 8.0%) vs. -1.2% (-0.1% from 7.8%).

- Decrease in required insulin units: -14.7% vs. -0.05%.

- FPG: -11.5% decrease (-0.95 from 8.2 mmol/L) vs. +2.5% (+0.2 from 7.87 mmol/L).

- PPG: -12.1% reduction (-1.3 from 10.7 mmol/L) vs. -1.25% (-0.13 from 10.4 mmol/L).

50 women diagnosed with PCOS (mean age 24.2, average BMI >31). [102]

1,000 mg/d berberine + 210 mg/d silymarin + usual diet and physical activity­­­.

6 months; open label, case control clinical trial.

At six months berberine and silymarin had improved insulin sensitivity, serum lipids and hyperandrogenism(p<0.01):

- HOMA IR: -22.2% (-1.2 from 4.4).

- Total cholesterol: -9% (-0.36 from 4.03 mmol/L).

- LDL: -9.9% (-0.2 from 2.09 mmol/L).

- Triglycerides: -4.2% (-0.05 from 1.35 mmol/L).

- Hyperandrogenism: Free testosterone (-15.4%) and free androgen index (-46%).

137 patients (mean age 57.9, BMI >29) experiencing adverse effects to statin medications (10 mg/d – 40 mg/d). [103]

1,000 mg/d berberine + 210 mg/d silymarin vs. placebo Both groups: half-dose of original statin medication + 600 kcal deficit diet.

6 months; double-blind RCT.

Compared to placebo, berberine and silymarin greatly minimised dyslipidaemia severity (

- Total cholesterol: placebo +19% (+0.91 from 4.8 mmol/L) vs. berberine and silymarin +4% (+0.2 from 4.9 mmol/L).

- LDL: placebo +22.5% (+0.72 from 3.2 mmol/L) vs. berberine and silymarin +2.7% (+0.09 from 3.34 mmol/L).

- Triglycerides placebo + 34.4% (+0.37 from 1.08 mmol/L) vs. berberine and silymarin +13.3% (+0.14 from 1.05 mmol/L).

Protective effects of berberine + silymarin over dyslipidaemia were associated with improvements in glucose metabolism markers, FPG, fasting insulin and improved HOMA IR (p<0.05).

Berberine

2,313 Chinese subjects (mean age 50) with T2DM. [104]




Variable dose of berberine (300 mg/d to 1.5 g/d vs. 1.5 g/d to 2 g/d vs. >2 g/d) either

alone, or in combination with oral hypoglycaemic agents (OHA) vs. placebo + OHA.

<90 days vs. 90 days vs. >90 days; systematic review and meta-analysis of 28 RCTs.

All berberine doses were effective compared to placebo (p<0.001), with added benefits when combined with medication (p<0.001). Outcomes observed were comparable with pharmaceutical treatment alone (p>0.05). Changes observed over 95 days (p<0.001):

- 0.3 g/d to 1.5 g/d berberine: -0.54 HbA1C, -0.38 mmol/L FPG and -0.71 mmol/L PPG.

- 1.5 g/d to 2 g/d berberine: -0.53 HbA1C, -0.70 mmol/L FPG and -1.34 mmol/L PPG.

- >2 g/d berberine: -0.64 HbA1C, -0.65 mmol/L FPG and -0.54 PPG.

4,158 T2DM patients (mean age 52.8, average BMI >24). [105]

90 mg/d – 9 g/d berberine (mean dose: 1,445 mg/d)

vs. either:

placebo (6 trials),

antidiabetic medication (46 trials), or

lifestyle intervention (4 trials).

4 to 48 weeks (mean duration 13.6 weeks); systematic review and meta-analysis of 46 RCTs.

36 studies: Berberine reduced HbA1c by -0.38, FPG by -0.58 and PPG by -1.48 (p<0.05). Combined with medication, berberine reduced HbA1c by -0.91 mmol/L, FPG by -1.06 mmol/L and PPG by -1.34 mmol/L (p<0.05). No significant difference was observed between berberine and antidiabetic treatments.

14 studies: HOMA IR was reduced by -0.71 points (p<0.05).

25 studies: Total cholesterol lowered by -0.64 mmol/L, LDL by -0.86 mmol/L, and serum triglycerides by -0.5 mmol/L. HDL was increased by +0.17 mmol/L (p<0.05).

15 studies: Mean BMI reduced by 1.07 (p<0.05).

Milk thistle

59 hyperglycaemic patients with T2DM (mean age 49.2, average BMI >29). [106]

200 mg/d silymarin

vs. placebo + 10 mg/d glibenclamide and diet control.

120 days; double-blind RCT.

Compared to placebo, silymarin treatment significantly reduced (p<0.05): FPG by -20% (-2.38 from 11.69 mmol/L), PPG by -36.8%, HbA1c by -16% (-1.46 from 8.9 %), and BMI by -9% (-2.71 from 31.6).

Chromium

64 diabetic patients with coronary heart disease (mean age 59.4, average BMI >29.9). [107]

200 μg/d chromium picolinate vs. placebo + aspirin and statins, antihypertensive or antidiabetic drugs.

12 weeks; double-blind RCT.

Chromium treatment achieved 900 g weight loss (p<0.003) compared to a 100 g gain with placebo, lowered BMI by -0.4 (p<0.006), FPG by -7.7% (-0.6 from 7.2 mmol/L; p<0.007) and plasma insulin by -12% (-1.4 from 11.6 μIU/mL; p<0.001). HOMA-IR was improved by -13% (-0.5 from 3.8; p<0.001), and hs-CRP was lowered by 13.5% (-0.7 mg/L decline from 5.2 mg/L).

64 PCOS patients (mean age 24.6, average BMI >25). [108]

200 μg/d of chromium picolinate vs. placebo.

8 weeks; double-blind RCT.

Chromium picolinate reduced elevated plasma insulin levels by -22.5% (-3.0 μIU/mL from 13.3 μIU/mL) vs. +28.5% with placebo (+3.1 μIU/mL; p<0.001). HOMA-IR was reduced by -25% (-0.7 points from 2.8 at baseline; p<0.001) vs. +32% increase with placebo. Chromium also reduced total cholesterol levels by -6.2% (-0.25 mmol/L from 4 mmol/L; p<0.03), and normal triglyceride levels by -12.5% (-0.15 mmol/L from 1.2 mmol/L; p<0.008).

92 PCOS patients (mean age 26.6, average BMI >28). [109]

200 μg/d of chromium picolinate vs. 1,500 mg/d metformin.

12 weeks; double-blind RCT.

Chromium picolinate decreased elevated fasting insulin by 9.3% (-1.51 μIU/mL from 16.2 μIU/mL; p<0.001) and achieved comparable effects to metformin on stimulating ovulation and supporting pregnancy rates.

25 overweight children (mean age 10.5, BMI >23). [110]

400 μg/d chromium chloride vs. placebo,

Both groups: nutritional education and aerobic exercise.

6 weeks; double-blind RCT.

Chromium supplementation reduced HOMA-IR by -51.6% (-1.84 points from 3.56; p<0.05) and lowered body fat by -2.84% compared to -0.39% with placebo.

Note: Pathology has been converted into millimoles per litre of blood (mmol/L) for Aus/NZ/universal interpretation.


Key: BMI: Body mass index; FPG: Fasting plasma glucose; HbA1c: Glycated haemoglobin; HOMA-IR: Homeostatic model assessment of insulin resistance; HDL: High-density lipoprotein; hs-CRP: High sensitivity C-reactive protein; Kcal: Kilocalories; LDL: Low-density lipoprotein; μg/d: Microgram per day; μIU/mL: Microinternational unit per millilitre; mg/L: Milligrams per litre; NS: Non-significant; PCOS: Polycystic ovarian syndrome; PPG: Post-prandial glucose; T2DM: Type 2 diabetes mellitus.


Table 2: Studies demonstrating berberine and silymarin safety in combination with metabolic medications.

Antidiabetic agents

Duration of berberine + silymarin treatment

Metformin [111],[112]

4 months

Metformin + DPP-4 inhibitor [††][113]

4 months

Metformin + sulfonylureas [114]

4 months

Metformin + pioglitazone [115]

4 months

Metformin + DPP-4 inhibitor+ pioglitazone [116]

4 months

Metformin + sulfonylureas+ DPP-4 inhibitor [117]

4 months

Sulfonylureas [118],[119]

3- 4 months

Sulfonylureas + DPP-4 inhibitor [120]

4 months

Metformin + DPP-4 inhibitor + pioglitazone [121]

4 months

Incretin [122]

3 months

Insulin [123],[124]

3-6 months

­­Glitazones [125]

3 months

Anti-cholesterol

HMG CoA-reductase inhibitors (e.g., simvastatin, rosuvastatin) [126]

3-6 months

Safety Information

Disclaimer: In the interest of supporting health Practitioners, all safety information provided at the time of publishing (Oct 2025) has been checked against authoritative sources. Please note that not all interactions have been listed.

For further information on specific interactions with health conditions and medications, refer to clinical support on 1800 777 648(AU), 0508 227 744(NZ) or via email, anz_clinicalsupport@metagenics.com, or via Live Chat www.metagenics.com.au, www.metagenics.co.nz


Pregnancy

  • Contraindicated.
    • Berberine binds to albumin and displaces bilirubin. Berberine has been linked to brain damage in a newborn with neonatal jaundice.

Breastfeeding

  • Contraindicated.
    • Berberine binds to albumin and displaces bilirubin. Berberine has led to brain damage in a newborn with neonatal jaundice.

Children

  • Likely unsafe. A review did not identify any concerns for use in children, however safety has not been conclusively established.


Prescribing Notes and Tips

  • Levothyroxine: Chromium might bind levothyroxine in the intestinal tract and decrease levothyroxine absorption. Advise to take Levothyroxine at least 30 minutes before or 3-4 hours after taking chromium.

Contraindications

  • Allergies and Sensitivities: Avoid in individuals with known allergy or hypersensitivity to members of the Asteraceae/Compositae family.
  • Hyperbilirubinaemia: Indian barberry contains berberine which binds to albumin displacing bilirubin. In those patients with hyperbilirubinaemia, use of berberine may cause an increase in unbound bilirubin. Avoid in those patients with hyperbilirubinaemia.

Cautions

  • Insulin and antidiabetic drugs: Milk thistle and berberine, a constituent of Indian barberry, exert blood sugar lowering effects whilst chromium may have insulin sensitising effects. This may theoretically lead to an additive hypoglycaemic effect when taken alongside insulin and antidiabetic drugs. Monitor those patients who are taking antidiabetic medications. This interaction may be beneficial, but individuals should continue to monitor their blood glucose.
  • GLP-1/GIP agonsists: Both chromium and GLP-1/GIP agonists lower blood sugar, so combining them increases the risk of hypoglycaemia.
  • Chemotherapy/Radiotherapy: It has generally been thought that antioxidants may interfere with chemotherapy and/or radiotherapy by decreasing the efficacy of the treatment, although recent studies have found that antioxidants are safe to use in conjunction with these treatments. However, it is still advisable to check with a patient’s oncologist before recommending a formula containing antioxidants.

Footnotes

[*] Energy storage sites are namely skeletal muscle and subcutaneous fat.

[†] ROS are unstable molecules containing oxygen which easily react with other molecules in a cell. A build-up of ROS in cells may cause damage to cellular deoxyribonucleic acid (DNA), ribonucleic acid (RNA) and proteins, and may cause cell death.

[‡] ER is a large, dynamic structure that serves many roles in the cell including calcium storage, protein synthesis and lipid metabolism.

[§] HDL:LDL ratios offer greater insight into dysfunctional metabolic patterns vs. isolated cholesterol parameters. Improvement in both HDL and LDL is linked to reduced hyperinsulinaemia following reduction of excess energy.

[**] In this study, berberine was observed to increase the activity of three key endogenous mitochondrial biogenesis factors: adenosine monophosphate kinase (AMPK), peroxisome proliferator activated receptor gamma coactivator 1-α (PGC- 1α) and SIRT1 in aged rats.

[††] DPP-4 (dipeptidyl peptidase-4) inhibitors are a recently introduced class of oral drugs for T2DM.


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