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Review

Milk Fat Depression in Dairy Cattle: Etiology, Prevention, and Recovery Approaches

by
Elena Niceas Martínez
1,
Rodrigo Muíño
1,
Joaquín Hernández Bermúdez
1,*,
Lucia Díaz González
2,
Jose Luis Benedito
1 and
Cristina Castillo
1
1
Department of Animal Pathology, Campus Terra-IBADER, University of Santiago de Compostela, 27002 Lugo, Spain
2
Department of Animal Pathology, Campus Terra, University of Santiago de Compostela, 27002 Lugo, Spain
*
Author to whom correspondence should be addressed.
Ruminants 2025, 5(3), 38; https://doi.org/10.3390/ruminants5030038
Submission received: 16 July 2025 / Revised: 8 August 2025 / Accepted: 11 August 2025 / Published: 12 August 2025

Simple Summary

Milk fat is a critical component of dairy products and a major determinant of the profitability of milk production. However, certain feeding strategies aimed at enhancing the nutritional quality of milk have unintentionally led to a condition known as milk fat depression (MFD), characterized by a significant reduction in milk fat content. This phenomenon may occur even though the total milk volume may remain unchanged or slightly increase, resulting in economic losses and concerns among dairy producers. For instance, using Galicia as an example, producers typically receive a bonus of 4 cents to 5 cents per liter per +0.1% increase in milk fat, above a reference threshold (usually 3.8%). MFD is primarily associated with dietary imbalances. These imbalances often lower the ruminal pH and alter microbial populations, disrupting fermentation and fatty acid metabolism. This review outlines the biological mechanisms underlying MFD and identifies its main nutritional causes. It also discusses current theories on how specific dietary fats and rumen microbiota interfere with milk fat synthesis. Finally, the review proposes practical strategies to prevent and mitigate MFD, including dietary modifications and targeted supplements: rumen buffers (magnesium oxide, sodium bicarbonate) to stabilize rumen pH; arginine (a nitric-oxide precursor) to support vasodilation and metabolic modulation; and vitamin E to provide antioxidant defense. Proper diet formulation remains the most effective and economical approach to preventing MFD, supporting both animal health and farm profitability.

Abstract

MFD is a nutritional disorder in dairy cattle characterized by a reduction in milk fat content despite a normal or increased milk yield. This review synthesizes current knowledge on the biological mechanisms and nutritional factors contributing to the development of this condition. Disruptions in rumen fermentation and alterations in fatty acid biohydrogenation (particularly the formation of trans-10 fatty acids) are recognized as central contributors to MFD. Several theories have been proposed to explain its pathophysiology, including the glucogenic, volatile fatty acid, trans fatty acid, and biohydrogenation theories. MFD is most commonly associated with diets low in fiber and high in polyunsaturated fatty acids or starch, which promote the accumulation of fatty acid intermediates that inhibit mammary lipogenesis. Among these, trans-10, cis-12 conjugated linoleic acid is particularly notable for its potent suppression of de novo fatty acid synthesis in the mammary gland. While proper dietary formulation remains the most effective preventive strategy, nutritional interventions such as magnesium-based alkalinizers, sodium bicarbonate, intravenous arginine, and vitamin E have shown promise in mitigating established cases. This review underscores the importance of nutritional management in preserving milk fat synthesis and promoting overall animal health.

1. Introduction

Recent research has increasingly focused on the role of diet (particularly the consumption of animal-derived products) in the development of chronic diseases such as cancer, cardiovascular disease, and insulin resistance [1,2]. Foods of animal origin, particularly those derived from ruminants, are a major source of dietary fat for humans. Ruminant fat is considered to be an important dietary component in many countries, with bovine milk fat alone accounting for up to 75% of the total fat consumption from ruminant animals [3,4]. Milk fat has been a target for modification primarily due to its association with human health and nutritional quality. Despite extensive study, important knowledge gaps remain, and further research to expand the evidence base is warranted [5]. Improving the nutritional quality of milk fat (particularly by increasing polyunsaturated fatty acids (PUFAs) and reducing saturated fatty acids (SFAs)) is a major focus in dairy nutrition, largely driven by growing consumer demand for healthier animal-derived products [4,5,6].
Effective strategies to prevent milk fat depression include dietary interventions, such as supplementing dairy ruminant diets with specific lipids and oil. Supplements rich in n-3 fatty acids and conjugated linoleic acids (CLAs) have been shown in both experimental and field studies to increase the levels of these bioactive compounds in milk and meat. Marine-derived lipids (including fish oils and algae) are particularly valuable because they contain eicosapentaenoic acid (EPA; C20:5(n-3)) and docosahexaenoic acid (DHA; C22:6(n-3)), which increase PUFA levels and improve the unsaturated-to-saturated fatty acid ratio in milk fat [7]. Plant-based lipids and by products from the oil and biofuel industries (corn, soybean, sunflower) also influence milk fat composition, although when combined with rich, rapidly fermentable carbohydrate diets, they may induce MFD [4,7]. Milk fat composition is also modulated by factors such as dietary intake, genetics, stage of lactation, mastitis, seasonal and regional variations, and ruminal fermentation [6]. Examples of inclusion levels and species in the cited experiments are as follows: an FO:SO blend at 45 g/kg DM (1:2; Holstein cows); tallow at 2% DM (Holstein cows); high-starch (342 g/kg DM) diets with NaHCO3 at 8 g/kg DM, MgO 4 g/kg DM, or dolomite at 8 g/kg DM (Holstein cows); vitamin E 12,000 IU/day with linseed oil (dairy cows); and intravenous arginine 0.216 mol in 4 L saline for 7 d (dairy cows). In studies combining monensin with dietary fat, soybean oil at 1.7% or 3.4% DM was fed to lactating cows [4,6,7].
The onset of MFD has become a significant concern for dairy producers due to the economic importance of milk fat and its variability in ruminants. As milk pricing systems increasingly reward a higher fat content, producers have shifted their focus toward optimizing milk fat synthesis and avoiding dietary practices that could compromise it [8]. The onset of MFD has become a significant concern for dairy producers due to the economic importance of milk fat and its variability in ruminants. As milk pricing systems increasingly reward a higher fat content [9], producers have shifted their focus toward optimizing milk fat synthesis and avoiding dietary practices that could compromise it. In many milk pricing systems, such as those used in Galicia (Spain), producers receive a bonus of approximately €0.04–0.05 per liter for each 0.1% increase in milk fat above a reference threshold (usually 3.8%), highlighting the economic relevance of maintaining an optimal fat content.
In response, extensive research efforts have been dedicated to understanding the mechanisms underlying MFD and identifying dietary triggers (particularly imbalances in fiber, starch, and unsaturated fat intake) that may contribute to its development [10,11]. Since 2001, nutritional guidelines have increasingly emphasized the importance of well-balanced diets to prevent metabolic disturbances such as MFD. These recommendations, as outlined by the National Research Council [12], emphasize the importance of maintaining appropriate ratios of digestible fiber, concentrates, and essential nutrients. In addition, feeding strategies must be adapted to the physiological and productive stage of the animal to ensure optimal rumen function and milk fat synthesis.
The aim of this review is to synthesize current knowledge on milk fat depression by critically evaluating the existing scientific literature and to outline evidence-based strategies for its prevention and management.

2. Milk Fat

Milk fatty acids (FAs) originate primarily from the diet and result from microbial activity in the rumen during the degradation of dietary lipids [13]. However, a substantial proportion of these FAs can also be synthesized de novo within the mammary gland. Milk fat consists of approximately 98% triacylglycerols (TAGs) [14], with around 70% being SFAs, 26% monounsaturated fatty acids (MUFAs), and 4% PUFAs [15]. Notably, at least 11% of the SFAs are short-chain fatty acids [16,17]. Further investigations have identified more than 400 individual FAs in milk fat, making it one of the most complex natural lipid matrices [13,15]. Milk provides high-quality protein and micronutrients; however, bovine milk fat is predominantly saturated. Typically, SFAs account for 65–70% of the total fatty acids (mainly palmitic (C16:0), myristic (C14:0), and stearic (C18:0)), while MUFAs contribute 25–30% (principally oleic acid, C18:1 cis-9), and PUFAs contribute 2–5% (notably linoleic, C18:2 n-6, and α-linolenic, C18:3 n-3). This composition has motivated nutritional and breeding/feeding strategies (also adopted by the food industry) to adjust the milk fatty-acid profile (increasing PUFAs or MUFAs and reducing specific SFAs) [5,6].
Approximately 40% of milk fatty acids are derived from dietary sources, 50% are synthesized de novo in the mammary gland, and 10% arise from lipolysis and mobilization of body fat reserves [18]. During negative energy balance, the contribution from mobilized body fat can increase to about 20% [18]. These proportions may vary depending on the species, breed, stage of lactation, and nutritional status. On the other hand, the origin of milk fat can also be determined based on the FA chain length: fatty acids with less than 16 carbons typically originate from de novo synthesis or lipid mobilization, whereas those with more than 16 carbon atoms are usually derived from dietary sources or mobilized fat, as illustrated in Figure 1 [19].
The complexity of milk fat is further influenced by multiple factors, including genetics, stage of lactation, mastitis, ruminal fermentation dynamics, and feeding strategies [15,21]. Seasonal variation also influences milk FA composition due to changes in nutrient quality and availability. During summer, pasture-based diets typically lead to a lower SFA content in milk fat, while winter feeding (often involving concentrate supplementation) results in higher SFA concentrations. Conversely, the proportion of unsaturated fatty acids (UFAs) tends to increase during summer and decrease in winter [22].
In regions such as northwestern Spain, where intensive and semi-extensive dairy systems predominate and rations are closely managed, seasonal effects are less pronounced. Nevertheless, alterations in any of the aforementioned factors (including genetics, lactation stage, mastitis, rumen fermentation, or diet) can contribute to the development of MFD. Taken together, these determinants not only shape the milk fatty-acid profile but, when sufficiently perturbed, can trigger a point we develop in the next section.

3. Milk Fat Depression Syndrome

MFD was first described over 150 years ago [23], and its definition has since been progressively refined. In this review, we define MFD as a reduction in milk fat yield (typically without a concurrent decrease in overall milk production or other milk components) accompanied by marked alterations in the milk fatty-acid profile [24]. For practical diagnosis, a milk fat concentration below 3.2% is often used as a working threshold [25,26], with herd, breed, and stage of lactation variability. The primary nutritional factor implicated in MFD is the disruption of normal ruminal biohydrogenation, particularly under dietary conditions involving a low forage and high concentrate or the inclusion of oils rich in PUFAs, such as fish oil [24]. Under these conditions, while milk volume and protein content typically remain unchanged, both the milk fat percentage and FA composition are markedly affected. Rivero [27] reinforced this concept by emphasizing that MFD is also characterized by alterations exceeding 50% in the milk FA profile.
However, Dewanckele et al. [7] challenged the rigidity of earlier definitions, noting that numerous studies have demonstrated that PUFA-rich supplements (such as fish or soybean oil) can reduce the milk fat concentration while simultaneously increasing overall milk yield [28,29,30,31,32]. This divergence underscores the need for a more nuanced and comprehensive understanding of MFD.
The alteration in milk fat composition during MFD is mainly driven by changes in ruminal biohydrogenation pathways, especially the trans-11 to trans-10 shift described by Davis and Brown [33]. In ruminants, dietary triacylglycerols are first hydrolyzed in the rumen, releasing free fatty acids. Unsaturated C18 fatty acids (linoleic, C18:2 n-6; α-linolenic, C18:3 n-3) undergo microbial biohydrogenation, which isomerizes double bonds and progressively hydrogenates them to trans-18:1 intermediates (predominantly trans-11 under typical conditions; trans-10 pathways are favored when the rumen pH is low and the dietary PUFA load is high) and finally to stearic acid (C18:0). These rumen processes determine the mix of ‘preformed’ FAs (>C16) delivered to the mammary gland and, via specific intermediates such as trans-10, cis-12 CLA, can secondarily suppress de novo synthesis (<C16). Consequently, ruminal fermentation has a central role in both the quantity and the quality (SFA/MUFA/PUFA profile) of milk fat [8,19,33].
However, attributing MFD solely to biohydrogenation is overly simplistic. Several theories attempt to explain MFD’s mechanisms, including the glucogenic theory [34], the volatile fatty acid (VFA) theory [35,36,37], and the trans-FA theory [33], all of which will be addressed in subsequent sections. According to the trans-10 shift hypothesis, an increase in trans-FAs within milk fat is a strong indicator of MFD. In grazing cattle, seasonal variation can influence the onset of MFD, especially in extensive systems where animals graze during spring and summer and receive energy-dense concentrates during winter. Nonetheless, in more intensively managed systems, such seasonal effects are less pronounced. Even so, pasture quality itself can fluctuate seasonally depending on crop maturity, species composition, and management. For example, the nutrient content may decline in poorly managed or flowering pastures, potentially inducing MFD at the end of spring or summer due to energy deficits [38], or even in early autumn [38,39]. Additionally, young pastures with abundant leaves and low structural carbohydrates often contain low fiber and high UFA concentrations, potentially contributing to MFD [27].
Typical MFD-inducing diets include those with high levels of concentrate or lipid supplementation alongside a reduced fiber intake. There is no single causative factor for MFD; instead, it appears to arise from complex interactions between diet and management practices [40]. These are summarized in Table 1.
These factors can be broadly categorized as follows:
  • Metabolic stressors, including the onset of lactation, inflammation, immune activation, and oxidative stress. Genetic background may further modulate these metabolic responses [42].
  • Nutritional stressors, such as high-starch or high-oil diets.
  • Non-nutritional stressors, including thermal stress (heat or cold), housing conditions, regrouping, and feeding behavior [20].
Among these, nutritional factors are the most extensively studied. Numerous studies have investigated the effects of PUFA-rich diets with a low neutral detergent fiber (NDF) content on milk fat yield and FA composition [10,43,44]. These conditions promote the accumulation of biohydrogenation intermediates that, once absorbed, can inhibit mammary fat synthesis [18]. In this context, the “trans-10 to trans-11 shift” denotes a change in the predominant trans-C18:1 positional isomer formed during rumen biohydrogenation (from trans-11 C18:1 (vaccenic acid) to trans-10 C18:1); a higher trans-10/trans-11 ratio is a practical indicator of altered biohydrogenation linked to the inhibition of mammary lipogenesis and MFD [18]. Specifically, such diets tend to reduce “de novo” FAs (<C16) while increasing the proportion of preformed FAs (>C16), reflecting a shift in mammary lipid metabolism [45,46,47]. The trans-10, cis-12 isomer of CLA, a known byproduct of altered rumen fermentation under low-fiber, high-oil feeding conditions, is one of the primary inhibitors of milk fat synthesis in the mammary gland [44,48].
Beyond marine unsaturated fats, saturated animal fats (particularly tallow) can also modulate milk fat composition by altering rumen biohydrogenation. When tallow is incorporated into maize silage based diets, concentrations of trans-C18:1 and other biohydrogenation intermediates in milk fat increase. Moreover, this feeding strategy has been associated with a shift toward the undesirable trans-10 biohydrogenation pathway. Onetti et al. [49] demonstrated that replacing half of the maize silage with alfalfa silage mitigated these negative effects. Consistently, trans-10 C18:1 concentrations were higher in cows fed corn-silage-plus-tallow diets than in those supplemented with alfalfa silage [41].
In conclusion, despite decades of investigation, the underlying mechanisms of MFD remain incompletely understood. Current evidence suggests that MFD results from complex interactions among dietary composition, rumen microbial dynamics, and mammary lipid metabolism. Comparative studies in other ruminants, such as goats, have also shown diet-induced changes in milk fat composition. It was demonstrated that the inclusion of sulla flexuosa hay in goat diets can improve milk fat composition and quality [50].

3.1. Theories on MFD Syndrome

Milk fat content can be influenced by multiple factors, with rumen microbiota playing a central role [50,51]. Certain rumen bacteria have been shown to induce the formation of trans-10 fatty acid isomers. For example, Kepler et al. [52] demonstrated that Butyrivibrio fibrisolven hydrogenates converts trans-10, cis-12 CLA to trans-10 18:1. Similarly, Megasphaera elsdenii YJ-4 produces trans-10, cis-12 CLA, while Propionibacterium from the mouse cecum can convert more than 50% of linoleic acid into trans-10, cis-12 CLA and approximately 10% to trans-10 18:1 [53]. Xue et al. [54] showed that the milk fat percentage decreases with lower rumen microbial richness, suggesting that disruption of ruminal symbiosis plays a key role in MFD. Nevertheless, the interaction between dietary structure and rumen fermentation is widely considered to be the primary cause of MFD [55,56,57].
Davis and Brown [32] classified MFD-inducing diets into two main types: (i) diets high in rapidly fermentable carbohydrates (RFCs) and/or low in physically effective fiber (peNDF), and (ii) diets supplemented with UFAs, particularly those rich in PUFAs such as marine lipids containing EPA (C20:5n-3) and DHA (C22:6n-3) [19]. Fiber in the diet is fermented by rumen bacteria into volatile fatty acids (VFAs), which are essential precursors for milk fat synthesis [58]. Interestingly, Si et al. [50] highlighted that milk fat may actually increase in animals fed high-fat diets, depending on VFA production and microbial adaptation.
Gaynor et al. [34] proposed two central theories to explain MFD: the “glucogenic theory” and the “trans-C18:1 fatty acid theory”. Bauman and Griinari [19] further refined this by classifying MFD mechanisms into two categories: (1) milk fat depletion due to limited precursors for lipid synthesis in the mammary gland, and (2) the presence of inhibitory substances that directly suppress milk fat synthesis. The first group includes the glucogenic and related VFA theories, while the second encompasses the trans fatty acid and biohydrogenation theories.

3.1.1. Milk Fat Depletion: Glucogenic Theory

First described by McClymont and Vallance [59] this theory, as illustrated in Figure 2 [34], posits that diets high in concentrates and low in forage elevate propionate production in the rumen, enhancing hepatic gluconeogenesis and insulin secretion while suppressing bovine somatotropin (bST). This hormonal shift reduces lipoprotein lipase (LPL) activity in the mammary gland and increases LPL activity in adipose tissue, diverting nutrients away from milk fat synthesis [34]. The result is nutrient partitioning that favors body fat over mammary lipid synthesis [19].

3.1.2. Substances with an Inhibitory Capacity for Milk Fat Synthesis in the Mammary Gland: Trans Fatty Acid Theory

This theory is based on the observed relationship between total trans-C18:1 fatty acids and MFD. Davis and Brown [33] were the first to propose this hypothesis. The presence of trans-C18:1 in milk fat indicates incomplete ruminal biohydrogenation of linoleic acid (C18:2) or linolenic acid (C18:3) [60]. Several studies have demonstrated that an increase in total trans-C18:1 in milk fat can result from a variety of diets already associated with MFD [34,61].

3.1.3. Substances with an Inhibitory Capacity for Milk Fat Synthesis in the Mammary Gland: Biohydrogenation Theory

To address the limitations of the trans-FA theory, Bauman and Griinari [24] proposed the biohydrogenation theory. It posits that dietary-induced alterations in rumen biohydrogenation pathways result in the formation of fatty acid intermediates with the capacity to inhibit mammary lipid synthesis. These intermediates, such as trans-10, cis-12 CLA, are absorbed post-ruminally and directly influence milk fat synthesis [7,44]. As is illustrated in Figure 3, the intermediates of the rumen biohydrogenation are trans-11 C18:2 (in the case of linolenic acid (C18:3)), and trans-11 C18:1 (when linoleic (C18:2) and linolenic acid (C18:3) are hydrogenated to stearic acid (C18:0)). The trans-11 C18:1 is the most abundant trans-isomer acid in milk fat composition, and due to its absorption from the duodenum into the bloodstream and its incorporation to milk fat, represented in Figure 3.
Other trans-C18:1 positional isomers are also incorporated into milk fat composition [62]. However, a key finding by another researcher demonstrated that MFD is more strongly associated with an increase in trans-10 C18:1 than with general trans-C18:1 isomers [63]. Several authors have expanded upon these results, establishing that when there is an increase in trans-10 C18:1 in milk fat, this is consistently linked to the diet causing MFD [64,65,66].
Biohydrogenation Intermediates Associated with MFD: Trans-10, Cis 12 CLA
As previously mentioned, trans-10, cis-12 CLA is a biohydrogenation intermediate generated when normal rumen fermentation pathways are disrupted by dietary changes. This fatty acid has been consistently detected in the rumen and milk of cows fed diets that induce MFD. Its inhibitory effect on milk fat synthesis has been confirmed by post-ruminal infusion trials, which showed a dose-dependent decline in milk fat content This FA has been consistently detected in both the rumen and milk of cows fed with diets that induce MFD [10,67]. Its inhibitory effect on milk fat synthesis has been confirmed through post-ruminal infusion trials, where it produced a dose-dependent decline in milk fat content [47,68]. Importantly, one of the defining characteristics of MFD is that the total milk yield often remains unchanged or may even increase, while the milk fat concentration significantly declines. This phenomenon has been observed in cows fed diets enriched with CLA or with high levels of starch and oils (HSO) [2,69]. Harvatine et al. [44], in a meta-analysis of 14 studies, supported the finding that the total milk yield is unaffected in cows subjected to an abomasal infusion of CLA, a conclusion further reinforced by Bayat et al. [70].
In controlled infusion studies, increasing doses of trans-10, cis-12 CLA (0, 3.5, 7.0, and 14.0 g/d) led to a marked reduction in de novo FA synthesis at the highest doses. At the lower dose (3.5 g/d), both de novo and preformed FAs decreased similarly [69]. Notably, even a small dietary inclusion (0.016% of dry matter) resulted in a 25% reduction in milk fat, and a strong negative linear relationship was established between CLA concentration and milk fat yield. However, Dewanckele [7] pointed out that trans-10, cis-12 CLA alone likely explains only about 3% of MFD cases, suggesting the involvement of additional inhibitory intermediates.
Biohydrogenation Intermediates Associated with MFD: Trans-10 18:1
This isomer has been associated with MFD due to its elevated concentration in milk fat when milk fat synthesis is suppressed [71]. However, Lock et al. [72] conducted a direct test using an abomasal infusion of trans-10 18:1 and found that it did not adversely affect milk fat synthesis. In that study, three groups were compared: a control group (ethanol infusion), a group infused with trans-10 18:1, and a positive control group infused with trans-10, cis-12 CLA. Only the latter group exhibited significant reductions in milk fat content (27%) and milk fat yield (24%). Although approximately 15% of the infused trans-10 18:1 was transferred into milk fat, it had no measurable inhibitory effect, thereby refuting its role as a causative agent of MFD [7].
Biohydrogenation Intermediates Associated with MFD: Cis-10, Trans-12 CLA
This fatty acid isomer has also been proposed to possess anti-lipogenic properties. Sæbø et al. [73] observed a modest reduction in milk fat when cows were abomasally infused with a mixture of cis-10, trans-12 CLA and trans-10, cis-12 CLA. While these findings suggested a potential synergistic or additive effect, no subsequent studies have confirmed the isolated role of cis-10, trans-12 CLA in MFD. As highlighted by Dewanckele et al. [7], there is currently insufficient evidence to support that cis-10, trans-12 CLA is a major contributing factor to MFD, particularly due to its inconsistent detection in affected cows.
Biohydrogenation Intermediates Associated with MFD: Trans-9, Cis-11 CLA
Another isomer of interest is trans-9, cis-11 CLA, which was evaluated through abomasal infusion at a dose of 5 g/day. This treatment resulted in a 15% reduction in both milk fat content and yield [74]. However, given its typically low concentration in milk fat (<0.10 g/100 g FA), it remains uncertain whether this isomer alone is sufficient to inhibit milk fat synthesis under typical dietary conditions.
In conclusion, although trans-10, cis-12 CLA remains the most consistently implicated intermediate in MFD, the syndrome likely results from a complex interplay among multiple biohydrogenation products, metabolic responses, and dietary factors.

4. Methods to Avoid and Mitigate MFD Syndrome

Recent studies have identified several strategies to prevent or mitigate MFD. In most cases, MFD arises from suboptimal dietary formulation (particularly rations high in PUFAs and low in fiber) that disrupt normal rumen function [19,24,75,76]. Therefore, the primary approach to preventing MFD is precise ration formulation that meets the nutritional requirements of dairy cows. Nevertheless, multiple contributing factors may also be involved [40]. According to NRC [12] guidelines, total mixed rations should include a minimum of 18% forage-derived NDF, 27% total NDF, at least 18% total dietary fat, and a maximum of 42% total NDF.
A recent study [77] demonstrated that supplementation with magnesium-based alkalinizers (calcium–magnesium dolomite and magnesium oxide) can effectively restore milk fat concentration within four days in cows affected by MFD. However, the beneficial effect subsided by the eighth day after supplementation ceased, emphasizing the need to correct the underlying dietary imbalance rather than relying solely on additives. These alkalinizers shift ruminal biohydrogenation of C18:2 away from trans-10 fatty acid production toward trans-11 fatty acid production, thereby restoring normal milk fat synthesis.
Another promising approach involves the intravenous infusion of the amino acid arginine (Arg). Ding et al. [78] reported that infusion of 0.216 mol of Arg in 4 L of saline for seven consecutive days increased both milk yield and milk fat production. This effect was attributed to elevated nitric oxide (NO) levels in the bloodstream, which enhanced mammary blood flow and nutrient delivery, ultimately stimulating de novo fatty acid synthesis in the mammary gland.
Similarly, sodium bicarbonate (NaHCO3), magnesium oxide (MgO), and calcium–magnesium carbonate (dolomite, CaMg(CO3)2) have been shown to effectively restore milk fat concentration in cows fed high-starch diets (342 g/kg DM) [78]. Such diets often induce subacute ruminal acidosis (pH < 5.8), which alters ruminal microbial populations and promotes the formation of trans-10, cis-12 CLA and other biohydrogenation intermediates known to inhibit milk fat synthesis. Among the three alkalinizing agents tested, sodium bicarbonate exerted the greatest effect on milk fat yield by increasing ruminal acetate production, a key precursor for de novo fatty acid synthesis. Nevertheless, both MgO and CaMg(CO3)2 also proved to be effective buffering agents [79].
Historically, monensin was used to enhance milk yield, despite its adverse effects on milk fat concentration, particularly in rations supplemented with soybean oil. Monensin alters rumen fermentation patterns, increases trans-10 FA production, and elevates the levels of inhibitory isomers such as cis-12 CLA and trans-9, cis-11 CLA [80]. Due to these undesirable effects and regulatory restrictions, monensin is no longer considered a viable strategy for the prevention or treatment of MFD. In Spain, its use is currently restricted to intraruminal boluses for the prevention of ketosis, although these devices have been temporarily withdrawn from the market [81].
Finally, some studies have reported that vitamin E supplementation may mitigate the negative impact of CLA on milk fat synthesis. Schäfers et al. [82] observed a protective effect, and Pottier et al. [83] demonstrated that supplementing 12,000 IU/day of vitamin E alongside linseed oil reduced the trans-11 to trans-10 shift in the rumen. This intervention led to a 17.93% increase in milk fat concentration, a 15.56% increase in milk fat yield, and a 47.06% decrease in trans-10 C18:1 content. This protective effect is attributed to the antioxidant capacity of vitamin E, which helps to preserve UFAs from oxidative degradation and may reduce their susceptibility to ruminal biohydrogenation. However, the authors emphasized that vitamin E is only effective when administered before the onset of the trans-10 shift; once the pathway is established, vitamin E cannot fully reverse MFD.
In conclusion, there are some implications for other bioactive compounds. Because fat-soluble vitamins and carotenoids are carried within the milk fat globule and its membrane, changes in fat secretion and rumen biohydrogenation that characterize MFD can coincide with shifts in these components. Diet remains the main factor: pasture quality and forage type influence vitamins A, E, and β-carotene in milk, and PUFA-rich diets can modify MFGM phospholipids, including sphingomyelin. Therefore, when MFD reduces milk fat yield, the total secretion per liter of fat-soluble compounds is expected to decrease if their concentration per unit of fat stays the same; however, direct evidence isolating MFD effects (independent of diet) is limited, so observed changes should be seen as diet-mediated rather than caused solely by MFD [84]. In contrast to rumen-focused MFD strategies, amino-acid infusion or rumen-protected AA (lysine, methionine) primarily increase milk protein synthesis and may improve milk protein (and in some cases fat) percentages, but they do not directly resolve MFD because they do not target the altered biohydrogenation state. We have clarified this in the text to avoid implying a causal link between AA supplementation and MFD alleviation [85,86].

5. Conclusions

MFD can be effectively prevented through the implementation of well-balanced and properly formulated rations that meet the physiological and nutritional requirements of dairy cows. Dietary fiber plays a critical role in maintaining optimal ruminal fermentation, supporting the production of key precursors for milk fat synthesis, and preventing disruptions in biohydrogenation pathways that could otherwise lead to the formation of fatty acids with inhibitory effects on the mammary gland.
When MFD is diagnosed, prompt dietary correction is essential. Additionally, several supplementary interventions have demonstrated the potential to accelerate recovery and mitigate economic losses. These include the use of magnesium-based buffers, intravenous arginine infusions, sodium bicarbonate (NaHCO3), magnesium oxide (MgO), calcium magnesium carbonate (dolomite, CaMg(CO3)2), and vitamin E, among others. While such strategies can be beneficial in restoring milk fat output, they should not replace the foundational importance of a properly formulated ration.
This review emphasizes that prevention remains the most effective and economically viable approach to managing MFD. A sound nutritional strategy not only minimizes the risk of MFD but also supports animal health, production efficiency, and overall farm profitability.

Author Contributions

E.N.M.: Writing—original draft, Methodology, Investigation; C.C.: Methodology, Investigation, Conceptualization, Supervision; J.H.B.: Methodology, Investigation, Conceptualization, Supervision, J.L.B.: Methodology, Investigation; L.D.G.: Methodology, Investigation; R.M.: Writing—review, and editing, Supervision, Conceptualization. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Informed Consent Statement

Not applicable.

Conflicts of Interest

The authors declare no conflicts of interest.

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Figure 1. Representation of milk fat composition and the origin of the fatty acids. Created in BioRender, https://biorender.com, accessed on 22 Jaunuary2025, based on Razzaghi et al. (2023) [20].
Figure 1. Representation of milk fat composition and the origin of the fatty acids. Created in BioRender, https://biorender.com, accessed on 22 Jaunuary2025, based on Razzaghi et al. (2023) [20].
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Figure 2. Impact of a low-fiber, high-fat ration on a cow’s metabolism. The glucogenic theory. Created in BioRender, https://biorender.com, accessed on 15 December 2024, based on data from Gaynor et al. (1995) [34].
Figure 2. Impact of a low-fiber, high-fat ration on a cow’s metabolism. The glucogenic theory. Created in BioRender, https://biorender.com, accessed on 15 December 2024, based on data from Gaynor et al. (1995) [34].
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Figure 3. Ruminal biohydrogenation of oleic, linoleic, and linolenic acid. Modified from Bauman and Griinari [24] and Dewanckele [7].
Figure 3. Ruminal biohydrogenation of oleic, linoleic, and linolenic acid. Modified from Bauman and Griinari [24] and Dewanckele [7].
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Table 1. Partial list of potential factors that may affect milk fat quantity and composition 1.
Table 1. Partial list of potential factors that may affect milk fat quantity and composition 1.
Rumen Environment AlterationPUFAs
Low pH/low peNDFAmount ingested (specially of linoleic acid (C18:2))
Feed particle size Availability
Fiber (amount and quality)PUFA/SFA ratio
Starch (non-structural carbohydrates)Feeding pattern
Rumensin (monensin) 2Variation in fat content and FA composition in feed
Feeding pattern
1 Adapted from Bauman [40] and Bauman [41]. 2 Banned in feed in Spain since 2003 according to Real Decreto 465/2003. Abbreviations: FA: fatty acid; PUFA: polyunsaturated fatty acid; SFA: saturated fatty acid; peNDF: physically effective neutral detergent fiber.
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Martínez, E.N.; Muíño, R.; Hernández Bermúdez, J.; Díaz González, L.; Benedito, J.L.; Castillo, C. Milk Fat Depression in Dairy Cattle: Etiology, Prevention, and Recovery Approaches. Ruminants 2025, 5, 38. https://doi.org/10.3390/ruminants5030038

AMA Style

Martínez EN, Muíño R, Hernández Bermúdez J, Díaz González L, Benedito JL, Castillo C. Milk Fat Depression in Dairy Cattle: Etiology, Prevention, and Recovery Approaches. Ruminants. 2025; 5(3):38. https://doi.org/10.3390/ruminants5030038

Chicago/Turabian Style

Martínez, Elena Niceas, Rodrigo Muíño, Joaquín Hernández Bermúdez, Lucia Díaz González, Jose Luis Benedito, and Cristina Castillo. 2025. "Milk Fat Depression in Dairy Cattle: Etiology, Prevention, and Recovery Approaches" Ruminants 5, no. 3: 38. https://doi.org/10.3390/ruminants5030038

APA Style

Martínez, E. N., Muíño, R., Hernández Bermúdez, J., Díaz González, L., Benedito, J. L., & Castillo, C. (2025). Milk Fat Depression in Dairy Cattle: Etiology, Prevention, and Recovery Approaches. Ruminants, 5(3), 38. https://doi.org/10.3390/ruminants5030038

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